Inhuman Experiment

Which Oils and Fats Are Best for Cooking?

noreply@blogger.com (JLL) — Mon, 21 Feb 2022 12:24:00 +0000

Avocado oil has the highest smoking point. (Photo by Muffet)

If you've wondered which oils and fats are the best choices for cooking your meals, this post is for you. The first question we need to ask is what makes an oil good or bad for cooking? Putting the cholesterol issue aside for a moment, we can say that perhaps the most important thing is how well the oil tolerates heat. We are using it for cooking, after all. Two factors that affect heat tolerance are smoking point and oxidation. Smoking point is, as you might have guessed, the temperature at which the oil begins to smoke. It's also the point the oil starts to break down chemically. This is something you generally want to avoid, so it's usually recommended that you don't heat the oil to its smoking point. This, of course, rules out using oils with a low smoking point for cooking at high temperatures. The second factor, oxidation, is related to smoking point in the sense that both are affected by temperature. However, oxidation also happens at lower temperatures than are needed for the oil to start smoking. Oxidation is problematic because the lipid peroxidation end-products (ALEs) it creates can wreak havoc inside the body. These products have been shown to accumulate with aging and cause problems such as liver spots on the skin. So which oils are most susceptible to oxidation? If you've read this blog before then you already know the answer: polyunsaturated fats. In fact, polyunsaturated fatty acids (or PUFAs) tolerate heat very poorly. Not only do they oxidize when you heat them on a frying pan, they do so inside the body as well. On the other hand, monounsaturated fats are much more resistant to oxidation than polyunsaturated fats. Saturated fats are the most resistant. This gives us a good rule of thumb when looking for fats to use in cooking: avoid oils high in polyunsaturated fatty acids. Because of their potential to undergo lipid peroxidation inside the body, I tend to restrict their consumption altogether, but even if you are a fan of vegetable oils and omega-3, using them for cooking is not a very good idea. The table above shows the relative percentages of saturated (SA), monounsaturated (MUFA) and polyunsaturated fatty acids (PUFA) in various cooking oils and fats (data from US and Finnish food databases). They are in a decreasing order of PUFA content, meaning that the oils moist suitable for cooking are on the left and the least suitable oils are on the right. Coconut oil has the highest SA content and the lowest PUFA content of all oils, making it very resistant to oxidation. Ghee and butter also have very little PUFA and lots of saturated fat. Based on this, butter is actually one of the best choices for cooking, although the high AGE content of butter and its tendency to brown quickly suggest to me that perhaps ghee is a better option. The reason might be that butter also contains some protein and a small amount of carbohydrate. Palm oil and lard are somewhat lower in saturated fat than the first three, but since their MUFA content is quite high, they still make good choices for cooking. The rest to the right of these five are less than optimal. Corn oil, sesame oil, rapeseed oil, peanut oil, and canola oil are all high in polyunsaturates, making them prone to lipid peroxidation. And unless you buy them cold-pressed, they will have been heated during refining anyway, so some oxidation has probably happened before you even use them. What about olive oil then? Even though everyone seems to love olive oil in general, there's something of a debate going on over whether it should be used for cooking purposes. My opinion is that, like the graph suggests, it's not the worst choice but it's not the best either. The smoking point of extra virgin olive oil seems to vary from 160 to 190 °C, depending on the free fatty acid content. Virgin olive oil, however, has some properties that make it more heat-tolerant than most other oils (link). In general, the less refined the oil, the lower the smoke point. Unrefined oils high in PUFAs have the lowest smoking points (link), but high saturated fatty acid content does not necessarily guarantee a high smoking point. Coconut oil, for example, has a fairly low smoking point (177 °C, about the same as butter and lard) compared to peanut oil (227 °C). Refined avocado oil, which is mostly monounsaturated fat, appears to have one of the highest smoking points at 255-270 °C (link). Ghee is another oil with a very high smoking point (252 °C). So which oils should you use for cooking? For sautéing and cooking at light to medium temperatures, my choice would be the ones on the left of the graph: coconut oil, ghee, butter, palm oil, and lard. If you stay below 170 °C, you're in pretty safe waters in terms of oxidation regardless of which one of them you choose. Virgin olive oil seems like a viable choice, too; just make sure the particular olive oil you're using it doesn't start smoking. For searing, browning and other methods of cooking requiring higher temperatures, ghee and avocado oil seem like the best choices. When it comes to resistance to oxidation, ghee might take the cake, but avocado oil appears to have the highest smoking point of all oils, even though it does have 13.5% PUFAs. Still, keep in mind that when cooking at very high temperatures, some advanced glycation end-products (AGEs) are bound to be generated. For more information on fats and health, see these posts: Coconut Lowers LDL, VLDL and Triglycerides, Raises HDL My Current Health Regimen Blood Test Analysis: The Cholesterol and Saturated Fat Issue Revisited Should Saturated Fat Be Avoided in Low-Carb Diets?

5 Reasons Why Dark Chocolate Is Better than Milk Chocolate

noreply@blogger.com (JLL) — Mon, 21 Feb 2022 12:23:00 +0000

Look good? Forget it, there's way too much sugar. (Photo by .craig)

You may have thought of chocolate as a guilty pleasure, but the ancient Maya considered it the food of gods. Granted, the Maya also thought cutting out someone's heart in a ritual ceremony was a good fun, but they did get one thing right: chocolate really is a health food. That is, as long as you buy the dark kind. In fact, the darker the chocolate the healthier it is. As good as that sugar-laden milk chocolate bar may taste, it wouldn't have made its way into any self-respecting Maya feast. If you don't believe me, read further for three good reasons to choose dark chocolate instead of milk chocolate. 1. Dark chocolate is better for weight loss. Even though the amount of calories in milk chocolate and dark chocolate are pretty similar (and in fact milk chocolate sometimes contains fewer calories), dark chocolate contains significantly less carbohydrates. Milk chocolate usually has about 50 grams of carbs per 100 g, while the amount of carbs in dark chocolate ranges from 8 to 35 carbs, depending on how dark it is. A chocolate with 70% cocoa has ~30 grams; a 85% chocolate has ~20 grams. If weight loss or maintenance is your goal, the combination of large amounts of carbohydrates and fat is something to avoid. A high carbohydrate load will increase insulin secretion, which is a signal for the body to store energy as fat. The reason why low-carb diets are so effective for weight loss is their effect on insulin: even if you eat lots of fat, if there are no carbs present to drive insulin up, the energy from dietary fat won't be stored into fat cells. Unless you consume only a small quantity or restrict other carb sources to a minimum, combining milk chocolate with a low-carb diet is going to be difficult. If your goal is to stay under 50 grams per day, 100 grams of milk chocolate fills up your entire quota. But 100 grams of 85% dark chocolate still leaves you with 30 grams to spend on other carb sources, making dark chocolate a viable option even for low-carb dieters. 2. Dark chocolate causes less aging. Okay, so perhaps a bit of an exaggeration there, since we don't know exactly how big a role advanced glycation end-products play in the aging process. We do know, however, that the accumulation of AGEs is one of the seven biomarkers of aging, which makes avoiding them a sensible goal. As it happens, weight gain is not the only problem with the carbs in milk chocolate. Almost all of the carbohydrate in chocolate is sucrose, which is half glucose and half fructose. Even though the word 'glycation' in 'AGE' implies that glucose is the culprit, the fact is that fructose is much more prone to cause AGEs in the body. Since the main ingredient in milk chocolate is sugar, a 100 grams of milk chocolate will also give you a hefty dose of fructose. Dark chocolate, on the other hand, is mostly composed of fat – cocoa butter, to be specific. The fatty acid composition is 61% saturated fat, 36% monounsaturated and only 3% polyunsaturated fat, making cocoa butter very resistant to oxidation. And if you're worried about cholesterol, here's something to ease your mind: almost all of the saturated fat in cocoa butter is cholesterol-neutral stearic acid. Fructose, however, may increase triglycerides levels. Unlike dark chocolate, milk chocolate also contains some lactose. In addition to making milk chocolate an impossible treat for some lactose intolerants, lactose also causes glycation. Lactose breaks down to glucose and galactose, and like fructose, galactose appears to form AGEs more rapidly than glucose. 3. Dark chocolate has more cocoa polyphenols. The health benefits of chocolate are almost entirely due to the polyphenols found in cocoa. As a rule of thumb, whenever you read something good about chocolate, what they're really talking about is cocoa. Therefore, as the cocoa content of chocolate increases, so do its positive effects on health. A standard milk chocolate will contain about 30% cocoa, while premium dark chocolates usually have more than 70%. Another thing that reduces the polyphenol content of chocolate (by 60-90%) is alkalization (link), also known as Dutch processing or simply Dutching. Alkalization was invented in the 19th century to get rid of some of the bitterness of cocoa powder and to make it more palatable. Non-alkalized cocoa powder is a more light brown in color and tastes less sweet than alkalized cocoa powder. Nowadays Dutch processing is very common among industrial chocolate makers (link), which suggests that there's a good chance the average high-sugar milk chocolate will contain alkalized cocoa. Many dark chocolates seem to use non-alkalized cocoa, however, probably because the bitterness is perceived as preferable among chocolate enthusiasts. 4. The cocoa polyphenols in dark chocolate are more bioavailable. Even if your dark chocolate happens to be made from alkalized cocoa, you'll still get more bang for your buck in terms of polyphenols, because the polyphenols will be more bioavailable. This is again related to differences in the macronutrient composition of chocolates. First, the bioavailability of cocoa polyphenols depends partly on the fat content of chocolate. One in vitro study showed that cocoa liquor (which is about 50% fat) retained more polyphenols than cocoa powder (about 15% fat) when submitted to a digestion model (link). The reason appears to be that the higher fat content increases the stability of cocoa polyphenols during digestion. Second, sucrose and milk protein may affect the absorption of polyphenols negatively (link). Dark chocolate contains no milk protein, less sucrose and much more cocoa liquor than milk chocolate. The actual content varies, since different countries have different regulations on what kind of chocolates can be called "dark chocolate". The FDA, for example, states that dark chocolate must contain at least 35% chocolate liquor, while milk chocolate only needs to have more than 10%. Also, chocolates with 40-70% cocoa are also sometimes sold as "dark chocolate", so be sure to check the ingredient list before purchase. The words "cocoa mass", "cocoa liquor", "cocoa powder", "cocoa paste", "cocoa solids", or something to that effect should be first on the list – if "sugar" is mentioned first, it's definitely not real dark chocolate. 5. Dark chocolate is more filling. Anyone who has tried both milk chocolate and dark chocolate must have noticed that it takes much less to satisfy chocolate cravings with the latter than the former. I can personally eat 200 grams of milk chocolate (more than 1,000 kcal) in one go without having my craving satisfied. With 99% dark chocolate, a few pieces is enough. A similar effect was shown in a study from last year (link). This, as mentioned before, is not related to energy content, because milk chocolate and dark chocolate have virtually the same amount of calories. Rather, the reason why a smaller quantity of dark chocolate is enough is probably a combination of less sugar and more nutrients. Humans generally have a preference for sweet foods, which is why we love candy when we're kids. But part of the reason why we can't stop eating candy until we feel sick is that there are no nutrients in candy, only calories. This lack of nutrients causes our body to send the satiety signal way too late. Since dark chocolate is higher in cocoa powder, it's also higher in many nutrients, such as iron, magnesium, phosphorus, copper and manganese. Combined with the lower amount of sugar and high amount of fat, it's no surprise you get your daily chocolate fix quicker with dark chocolate than milk chocolate. Summary Dark chocolate contains less sugar, more cholesterol-neutral fat, and more cocoa polyphenols in a more bioavailable form than milk chocolate. Dark chocolate is also more filling, which means it takes less calories to satisfy your chocolate cravings. Keep in mind, however, that excess consumption of dark chocolate has its downsides too. Cocoa powder is high in iron and oxalates, which are harmful in high quantities. We'll return to the subject of optimal intakes in future posts, but for now, I limit mine to 50-100 grams of chocolate per day. For more information on chocolate, sugar, fat, and health, see these posts: Tea, Coffee and Cocoa: All Good for Your Teeth SAs, MUFAs vs. PUFAs: Fat Storage Depends on Type of Fatty Acid in Rabbits Fats and AGEs: PUFAs Are Even Worse than Fructose Low-Carb vs. Low-Fat: Effects on Weight Loss and Cholesterol in Overweight Men

Soy Isoflavones Grow Hair by Increasing IGF-1 in the Skin

noreply@blogger.com (JLL) — Sun, 20 Feb 2022 11:31:00 +0000

Food sources of isoflavones include tofu and miso soup. (Photo by sokole oko)

Many of you have probably heard that soy isoflavones may be good for hair loss. How exactly dietary isoflavones work to promote hair growth is less clear, however. In male rats even a relatively low amount of soy isoflavones reduces DHT and increases testosterone. This alone would probably be enough to explain hair growth in rodents. Of course, humans are a more difficult case. Most of the things that show promise in mice or rats don't work for humans with androgenic alopecia in the end. The good news is that soy isoflavones reduce DHT even in humans. The bad news is that the reduction may not be great enough. About 60 mg of isoflavones daily reduced serum DHT in healthy young men by only 15%. Even this moderate drop would suggest a reduction in 5-alpha-reductase, which converts testosterone to DHT. However, the markers of 5-alpha-reductase looked at in the study did not show a difference between the treated and the control group. And yet, a combination of capsaicin and soy isoflavones grows hair in both animals and humans. In this study, capsaicin injected into the skin was enough to grow hair in animals, although the combination was more effective. In humans, orally administered isoflavones and capsaicin resulted in hair growth in 88% of the participants with androgenic alopecia, which is a remarkable result for a supplement that reduces DHT by so little. The authors speculated that capsaicin and soy isoflavones promote hair growth by increasing dermal levels of insulin-like growth factor (IGF-1). They suggested that a key factor was calcitonin gene-related peptide (CGRP), which acts as a vasodilator, among other things. It also increases IGF-1 in various tissues, including the skin. This theory is supported by the fact that subcutaneous capsaicin increased CGRP release and IGF-1 expression in hair follicle cells in normal mice but not in CGRP-knockout mice. Soy isoflavones increased the production of CGRP, which explains why the combination was more effective than capsaicin alone. Based on these studies, it was still unclear whether dietary isoflavones alone promote hair growth. Now, the same authors have investigated their idea further. In their new study, they fed isoflavones to mice whose backs were shaved and measured their hair growth (link). Again, both wild-type mice and CGRP-knockout were used. The isoflavone supplement used was Fujiflavone P40, which contains 43.5% isoflavones. 5 g of the product was mixed per each kg of standard chow. On average, the mice ate 4.6 grams of food daily, which means that their daily intake of isoflavones was 0.0046 * 0.005 * 0.435 = ~10 mg (correct me if my calculation is wrong). After three weeks of isoflavone administration, dermal CGRP and IGF-1 levels in wild-type mice increased significantly compared to the control group. In the knockout mice, no difference was seen between mice given isoflavones and the control group. Hair follicle number also increased in wild-type mice given isoflavones. Compared to the control group, they had about 40% more hair follicles. The knockout mice had less hair follicles to begin with, and when they were given isoflavones, no improvement was seen. Thus, it seems that isoflavones grow new hairs through increasing dermal levels of CGRP and IGF-1. Compared to the mice given isoflavones, the control mice seemed to take a longer time growing their existing hair back. Even the knockout mice that saw no increase in IGF-1 grew their hair back quicker when they were given isoflavones. This might be due to other effects of isoflavones, such as reducing DHT levels. Based on the pictures in the full paper, the wild-type mice grew their hair back even quicker, however. Wild-type mice given isoflavones also had a more pronounced darkening of hair than their control group. So what is the take home message? Based on all these studies, it looks like soy isoflavones show very good potential for promoting hair growth. A part of their effectiveness may come from the fact that they reduce serum DHT and increase testosterone, but based on the rodent data, the real kick is from the increase in skin levels of IGF-1. At the moment, there is no data comparing the effectiveness of soy isoflavones vs. capsaicin in humans. However, we do know that the combination is superior in increasing dermal IGF-1 in animals, and that the combination of both taken orally grows hair in humans with androgenic alopecia. For more information on hair growth, see these posts: Topical Retinoids Increase Hair Growth in Most People BioSil, JarroSil & Beer – Silicon Experiment Conclusion Zinc Pyrithione Reduces Shedding and Moderately Promotes Hair Growth Hair Growth with Ayurveda – The Nutrich Oil Experiment

Topical Retinoids Increase Hair Growth in Most People

noreply@blogger.com (JLL) — Thu, 17 Feb 2022 14:22:00 +0000

Retinoids – slap them on your scalp and let nature do the rest. (Photo by Steve Rhode)

Retinoid creams and gels are probably the most effective skin care products out there at the moment. They seem to do just about everything you could hope for: increase skin firmness and hydration, reduce wrinkles, improve skin tone, you name it. But what about hair growth? The effects of retinoids on hair growth have been much less studied, even though the positive data on skin health suggests they might rejuvenate scalp skin also. My own experiment with retinol (the milder cousin of retinoids) and the resulting new hairs certainly supports this idea. And yet, while my ongoing experiment with tretinoin has visibly improved my skin, I can't say I've seen much of an increase in hair growth. I find this somewhat surprising, given that tretinoin is much stronger than retinol. Time to take a look at what the science says on retinoids and hair growth. The earliest paper I could find compared the effects of various treatments on hair regrowth in mice (link). According to the paper, retinoic acid applied topically was the least effective of the three treatments but still caused some hair regrowth after shaving the backs of the mice. Interestingly, UV irradiation was more effective, while estradiol suppressed hair regrowth. Then, in 1986, a group of scientists decided to try topical retinoids and minoxidil on humans with androgenic alopecia (link). After one year of using the combination, 66% of the participants saw regrowth of terminal hairs. None of the participants used minoxidil alone, but some of them did use only retinoids. Applying 0.025% tretinoin topically resulted in hair growth in 58% of the subjects. The picture below shows one subject before and after using tretinoin. According to the authors, the hair growth may be due to increased cell proliferation and differentation and the generation of new blood vessels. Another paper that appeared a few years later also speculates on how retinoids might cause hair growth (link). The authors of this paper suggest that certain retinoids increase the rate of hair of hair growth, prolong the anagen phase, and help convert vellus hairs to terminal hairs. At least in mice, levels of cellular retinoic acid binding protein are higher during the anagen phase and lower during the telogen phase of hair growth. Applying some retinoids topically increases the level of this protein in the skin, which might explain how retinoids prolong the growth phase (link). Both isotretinoin (also called 13-cis-retinoic acid) and tretinoin (also called all-trans-retinoic acid) seem to shorten the telogen phase and increase the anagen phase; however, they also differ in their effects, at least in vitro (link). A review on retinoids and hair growth states that according to the studies, only tretinoin and isotretinoin are able to prolong the anagen phase (link). I'm not sure how true this statement is, given that other vitamin A derivatives such as etretinate have been associated with hair darkening and new hair growth (link) and even retinol boosts the effectiveness of minoxidil (link). Not all studies have found the combination of minoxidil and retinoids to be superior to minoxidil alone (link). The hypothesis that retinol and some retinoids increase the absorption of minoxidil is plausible, but this is not the only explanation, since retinoids are effective even on their own. Thus, with or without minoxidil, retinol and retinoids seem worth a shot. Keep in mind, though, that the picture above shows the result after one year of use, and that almost half of the participants did not see an increase in hair growth. For more information on hair growth, see these posts: Zinc Pyrithione Reduces Shedding and Moderately Promotes Hair Growth Hair Growth with Ayurveda – The Nutrich Oil Experiment Do Flax Lignans Reduce Hair Loss from MPB? Green Tea Extract Grows Hair in Vitro, Might Work in Vivo

Refined vs Red Palm Oil and Cholesterol

noreply@blogger.com (JLL) — Thu, 17 Feb 2022 14:21:00 +0000

Palm oil, palm kernel oil, palm olein and palm stearin are all different products of the palm tree.

Palm oil is extracted from the pulp of the fruit of the oil palm. Palm kernel oil, on the other hand, is extracted from the seed of the oil palm. While red palm oil (also known as crude palm oil) is easily distinguishable by its deep orange to red color, refined palm oil and palm kernel oil can be hard to tell apart. Both are white to yellowish in color and solid at room temperature.

Palm oil contains about 45 g saturated, 40 g monounsaturated, and 8 g polyunsaturated fatty acids per 100 grams. Though not as saturated as coconut oil, palm oil is still at the top of the list when it comes to saturation. Palm kernel oil is even more saturated, containing more than 80% saturated fatty acids.

It's no surprise that palm oil has been labeled an unhealthy fat by most health experts. Obviously, this much saturated fat must send cholesterol levels through the roof and, as a result, cause heart disease. Right?

Well, not quite. After going through pubmed for all the abstracts (and a couple of full papers) on palm oil and cholesterol, it's clear that the case is everything but clear. The heart disease part deserves it's own post, but for now let's concentrate on how palm oil really affects cholesterol levels.

Palm oil and cholesterol in animals

In one study, partially refined, bleached and deodorized (RBD) palm oil was fed to rats on different diets (link). All groups that were given palm oil as part of their diet had significantly lower total cholesterol (TC) levels than the control group. In addition, when normal and hyperlipidemic rats were given palm oil, they had higher HDL levels than hyperlipidemic rats that were not fed palm oil. Similar results were seen in another study where rats given palm oil had a higher ratio of HDL to total cholesterol and lower triglycerides than the control rats (link).

An earlier study that fed rats with various fats for a year came to a different conclusion (link). TC was higher in rats fed palm oil than in rats fed with other fats such as sunflower oil or butter. Triglycerides were higher in palm oil and butter groups than in sunflower oil groups. And, to make things even more confusing, rats fed palm oil for four weeks showed a tendency for slightly lower triglycerides and HDL, whereas sunflower oil tended to increase triglycerides and HDL (link).

Basically what the above studies show is that the results vary greatly. Sometimes palm oil improves TC/HDL ratio, sometimes it worsens it. Sometimes triglycerides decrease, sometimes they increase. What's more, these two don't even have to go hand in hand, which makes it hard to decide whether the overall effect is good or bad.

One question that raises at this point is whether refining the oil makes a difference. One study that compared unrefined (that is, red/crude) and refined palm oil found that rats fed unrefined palm oil had lower total cholesterol, LDL, VLDL and higher HDL than those fed refined palm oil (link). Perhaps the tocotrienols in red palm oil play a role? Maybe so, but there is also one study that did not see a difference in cholesterol levels between rats fed red palm oil and refined palm oil for three months (link).

There are also other variables that might affect the end results. For example, I found one rat study that directly compared the effects of fresh and once or repeatedly heated palm oil (link). The rats that were given either fresh or once-heated palm oil did not have any deleterious effect, whereas palm oil heated five times increased total cholesterol and thiobarbituric acid reactive substances (TBARS) levels. This means that even though palm oil tolerates heat much better than most oils, using the same oil many times may not be a good idea.

Similarly, comparing fresh and oxidized (either through heating or prolonged exposure to air) palm oil shows that while both increase total cholesterol compared to rats eating a normal diet, oxidized palm oil increases it even more, and that this is due to an increase in LDL, not HDL (link). Further, oxidized palm oil increased the mean arterial blood pressure of the rats, while fresh palm oil did not.

Unlike humans, hamsters fed oil and dietary cholesterol quickly develop hyperlipidemia. Hamsters that were given various palm oils had dramatically lower levels of total cholesterol, LDL and VLDL than hamsters given coconut oil (link). The three forms of palm oil were red palm oil, refined palm oil and refined palm oil with red palm oil extract. In the hamsters that were fed red palm oil or refined palm oil with red palm oil extract, HDL levels were significantly higher and triglycerides significantly lower than in hamsters fed coconut oil.

The best one of the three was unrefined red palm oil, but as you can see, even refined palm oil had favourable effects. Note also that adding an extract of red palm oil into the refined palm oil improved things, which supports the idea that the carotenoids, tocotrienols and tocopherols play a role in the health effects of red palm oil.

In another study, hamsters given palm oil had higher levels of total cholesterol, HDL and triglycerides than those given olive oil or maize oil (link). The title of the paper suggests that the amount saturated fat is directly responsible for HDL levels in hamsters: when they eat little saturated fat, HDL is low, and vice versa. However, in the previous study HDL increased after switching from coconut oil to red palm oil, even though coconut oil is higher in saturated fat.

In vervet monkeys, palm olein oil reduced the risk the risk for developing early atherosclerotic lesions while not significantly affecting cholesterol levels compared to monkeys given lard or sunflower oil (link). Note, however, that palm olein oil is not the same as palm oil. Although it has a high palmitic acid content like palm oil, palm olein oil is the refined, liquid fraction of palm oil. The solid fraction is palm stearin. Palm olein is about 45% saturated and 55% unsaturated, while palm stearin is 60% saturated and 40% unsaturated. While they may have different effects, at least in rats palm stearin, palm olein and palm oil all increased HDL in one study (link).

Palm oil and cholesterol in humans

While animal studies may give us an idea of what to expect, we are not rats, hamsters or monkeys. Humans are adapted to a different kind of diet through evolution, and cholesterol studies in animals can be pretty misleading when applied to humans.

First, let's take a look at what happens when you give palm oil to people with what doctors would call hypercholesterolemia or high cholesterol. In women with high cholesterol, soybean oil, rice bran oil and palm oil all reduced LDL and TC, despite their differing fatty acid composition (link). Thus, saturated fat does not necessarily increase LDL.

In this study, only soybean oil reduced HDL. Soybean oil also reduced small dense LDL (sd-LDL), while palm oil consumption increased it. That same LDL was more susceptible to oxidation in those who consumed soybean oil, however. Since oxidized LDL appears to be the best predictor of atherosclerosis, perhaps an increased number of small LDL particles with less oxidation is better than increased oxidation with less particles.

When older women with high cholesterol were given sunflower oil (which is very high in PUFA) or palm olein, the latter increased total cholesterol and LDL, especially in women with high TC to begin with (link). Contrast this with the previous study where the palm oil normalized cholesterol levels. Still, no difference was seen in TC/HDL ratio. HDL increased only in those with normal cholesterol levels. Again, palm olein also decreased LDL oxidation, especially in those with high cholesterol.

There's also a study that compared sunflower oil and palm olein in older women but with normal cholesterol. This time, the diet containing palm olein increased TC and HDL compared to a sunflower oil diet (link). Another study found palm oil and sunflower oil to cause no difference in HDL, whereas palm oil increased TC and LDL (link). A third comparison of the two oils found the same (link).

Perhaps palm oil and palm olein have different effects on cholesterol? That sounds plausible, but one study found no difference between palm oil, palm olein, palm stearin and soybean oil in terms of LDL, HDL and triglycerides (link). Then again, not all palm oleins are equal. When red palm olein and palm olein was compared with sunflower oil in patients with excessive fibrinogen (a blood clotting factor) in their blood, red palm olein came out on top (link). Palm olein increased TC more than red palm olein and sunflower oil. LDL increased in the palm olein group compared to the sunflower oil group.

So far, we've looked at palm oil vs. PUFA-rich oils, but what about other fats? Lard has a pretty similar fatty acid profile as palm oil. It has plenty of MUFAs and SFAs but only little PUFAs. Comparing palm oil with soybean oil, peanut oil and lard in Chinese adults showed that palm oil reduced TC and LDL, while lard increased both (link). Peanut oil had no effect. Palm oil also improved the TC/HDL ratio.

A study that fed palm oil, lard or puff-pastry margarine to obese women found no difference in cholesterol levels (link). It did find that obese women had lower HDL levels and higher fasting leptin (four times as high!) than normal-weight women, however. So, compared to lard, palm oil either reduces LDL or does nothing.

Peanut oil is 49% MUFA, 33% PUFA and only 18% SFA. The MUFA content is similar to palm oil but its PUFA content is much higher. One study found no difference between palm olein from red palm oil and peanut oil (link). Olive oil is even higher than peanut oil in MUFA, containing about 70% of its fatty acids in the monounsaturated form. One study found no difference between palm olein containing tocotrienols and olive oil in terms of cholesterol (link).

Coconut oil is much higher in saturated fat than palm oil. Unsurprisingly, it tends to raise cholesterol in most animal studies more than other fats. In humans, small amounts may not make a big difference. Enriching the diets of healthy, young women with palm oil or coconut oil did not result in differences in total cholesterol compared to consuming the same amount of energy MUFAs (link). In larger amounts the difference start to become clearer. Compared to coconut oil, palm oil generally results in lower total cholesterol, LDL and HDL (link).

Still, even high amounts of red palm oil doesn't necessarily increase cholesterol. In Chinese men, a diet containing 28% fat with red palm oil accounting for 60% of that, no change was seen in total cholesterol, triglycerides, or HDL after 42 days (link). Plasma concentrations of carotenoids and vitamin E increased, however.

Hydrogenation, which turns liquid fats solid, may also play a role. Compared to saturated fatty acids such as palmitic acid, hydrogenated fats containing trans fatty acids tend to increase total cholesterol and LDL while lowering HDL levels (link, link). One paper compared the effects of palm oil with partially hydrogenated fat and oils high in MUFAs or PUFAs (link). Partially hydrogenated soybean oil and palm oil resulted in higher LDL than regular soybean oil. There was no significant difference in TC/HDL between the oils, but HDL3 was higher after palm oil.

In another study, three different margarines were given to 27 young women (link). One of the margarines was based on palm oil, one on partially hydrogenated soybean oil and one was made with a high content of PUFAs. The PUFA margarine lowered total cholesterol and LDL compared to the other two, while soybean margarine lowered HDL compared to the other two. One study compared the effects of partially hydrogenated soybean oil, high oleic palm olein and unhydrogenated palm stearin (link). Both soybean oil and palm stearin increased TC/HDL compared to palm olein, with palm stearin having a lesser effect than soybean oil.

Looking at the question from the opposite angle gives similar answers. The saturated fat in a typical Dutch diet comes mainly from animal fats and hydrogenated oils. Replacing them with palm oil resulted in an 11% increase in HDL and a 8% decrease in the LDL/HDL ratio (link). Triglycerides were also reduced.

In many of the studies, the subjects are either given supplements or they just basically scoop up the fat with a spoon. This is not how most people actually use these oils, however – they cook with them. When you put different oils into a frying pan and then eat them is when you start to see different results.

For example, using palm oil or soybean oil for cooking does not seem to change serum cholesterol levels much in the short term (link). However, cooking in soybean oil resulted in a 47% increase in triglycerides compared to palm oil, which goes to show that oils high in PUFAs are not very suitable for cooking. Also, some of the effects may only become visible after a longer period of time. There aren't many long-term studies in humans, but Mauritius is an exception. In 1987, the government changed the formula of the commonly used cooking oil from palm oil to soybean oil. As a result, total cholesterol levels dropped by about 0.8 mmol/L in the course of five years (link). There's no mention of triglycerides, unfortunately.

Finally, men and women seem to respond differently to dietary fats. When a small amount of red palm oil was given to healthy subjects for two weeks, all lipid fractions decreased, with a statistically significant decrease seen in LDL and triglycerides (link). A closer look revealed that there was a difference between men and women, however: in men, LDL actually increased mildly.

One study looked at the effects of palm oil in the context of high and low dietary cholesterol (link). Diets high in palm oil slightly increased total cholesterol and LDL with no significant changes in HDL or triglycerides. Interestingly, diets low or moderate in palm oil increased total cholesterol and LDL much more than the diets high in palm oil, even when the high-palm oil group consumed more eggs.

Tocotrienols are generally considered to have a cholesterol-lowering effect (link). The effects of tocotrienol supplements on cholesterol are not conistent, however (link, link). A possible explanation is that alpha-tocopherol might attenuate some of the cholesterol-lowering effect of tocotrienols (link).

Medium-chain triacylglycerods (MCTs) are usually thought to have a neutral effect on cholesterol, but a comparison of MCTs with palm oil and high oleic acid sunflower oil showed that MCT and palm oil had a similar effect (link). Sunflower oil resulted in lower total cholesterol. The authors conclude that "this study suggests that medium-chain fatty acids have one-half the potency that palmitic acid has at raising total and LDL-cholesterol concentrations."

Summary

So what do we make of all this? As I'm sure you noticed, there's a lot of different kinds of studies and a lot of conflicting data out there when it comes to palm oil and cholesterol. Some common themes appear in the results, however:

Compared to PUFA-rich oils, palm oil increases TC in most human studies
Compared to MUFA-rich oils, palm oil behaves neutrally in most human studies
Compared to SFA-rich oils, palm oil reduces TC in most human studies
In animals, palm oil tends to increase HDL and lower triglycerides
In humans, palm oil tends to increase LDL, at least in men
Palm oil makes LDL less susceptible to oxidation
Small amounts of palm oil don't make much of a difference either way
Palm oil tolerates cooking well, but don't use the same oil more than once
Red palm oil seems to have a more neutral effect than refined palm oil

Just from a cholesterol perspective, palm oil doesn't look all that bad – and we haven't even looked at how palm oil consumption affects cardiac risk! Although some conflicting evidence exists, in most of the studies the effect on cholesterol is closely related to the fatty acid composition of the oil.

Thus, when you compare palm oil with sunflower oil, you're most likely going to see an increase in total cholesterol, since polyunsaturated fatty acids tend to lower cholesterol compared to saturated fatty acids. Monounsaturated seem neutral in most cases. Still, keep in mind that individual fatty acids behave slightly differently. The high palmitic acid content of palm oil may explain why HDL levels are unchanged in many human studies.

One thing to remember is that if you use the oils straight from the bottle (e.g. on top of a salad), the difference between sunflower oil and palm oil may not be that great. However, if you use them for cooking, picking an oil high in PUFAs is asking for trouble. Saturated fats such as palm oil are less susceptible to oxidation and also make (the possibly increased) LDL less susceptible to oxidation.

Finally, while refined palm oil is most likely a better choice for cooking than less saturated fats, go for red palm oil whenever you can. Not all studies have shown a significant difference in cholesterol levels between red palm oil and refined palm oil, but some have, and tocotrienols have plenty of other health benefits as well.

What a "Heart-Healthy" Diet Does to Your Cholesterol Levels
5 Reasons Why Dark Chocolate Is Better than Milk Chocolate
Should Saturated Fat Be Avoided in Low-Carb Diets?
Coconut Lowers LDL, VLDL and Triglycerides, Raises HDL

AGE Content of Foods

noreply@blogger.com (JLL) — Sun, 06 Feb 2022 13:23:00 +0000

Hot dogs are high in AGEs. (Photo by TheBusyBrain)

There are two ways that advanced glycation endproducts (AGEs) are formed: inside the body or outside the body. These are known as endogenous and exogenous AGEs, respectively. The accumulation of AGEs is one of the seven types of aging damage. While it's uncertain just how big a role exogenous crosslinks play in aging, consuming excess amounts of AGEs through diet has been shown to cause serious health problems in animals and humans. Therefore, it seems useful to have some idea of which foods are especially high in AGEs. The following is a list of the AGE contents of commonly consumed foods. The data is based on one study (link). The authors state:

Two-hundred fifty foods were tested for their content in a common AGE marker (epsilon)N-carboxymethyllysine (CML), using an enzyme-linked immunosorbent assay based on an anti-CML monoclonal antibody. Lipid and protein AGEs were represented in units of AGEs per gram of food. -- -- A limitation of the present data is reliance on CML, a single AGE marker, while many other AGEs/ALEs are generated in food, albeit of unknown significance. In practical terms, however, CML is a commonly measured AGE/ALE compound, used routinely as an indicator of the AGE/ALE burden in numerous animal and human studies

Other ways of measuring AGEs might produce different values, so the numbers below serve mostly to give a rough idea of the relative AGE contents of foods. If you want to compare your own intake with others, here's a quote from the full paper:

In a preliminary survey of the usual daily AGE intake, we analyzed 3-day food records from healthy individuals (n=34). Mean daily AGE intake was 16,000±5,000 kU AGE. These data were used to define a high- or low-AGE diet, depending on whether the estimated daily AGE intake is significantly greater or less than 16,000 kU AGE. A similar investigation in 40 type 2 diabetic patients showed a daily AGE intake of 18,000±7,000 kU AGE, with major proportions of AGE contributed by broiled, fried, grilled, and roasted meat and meat alternatives.

So anything above 16,000 kU (see the list below for values) per day would put you in the high-AGE category. Again, keep in mind that we are talking about crosslinks produces outside body; whatever happens once the foods are digested, important as it may be, is beyond the scope of this post. Based on the data, we can make the following generalizations:

Fats and meat products contain the most AGEs
Carbohydrates are relatively low in AGEs
Higher cooking temperatures increase AGEs
Longer cooking times increase AGEs
The presence of liquids in cooking reduces AGEs
Processed foods have more AGEs than natural or homemade foods

I will try to keep this post updated as I come across new data to include in the list, so remember to check back every now and then. Below, AGEs are expressed either as units per gram (for solids) or units per milliliter (for liquids). Serving sizes are grams, and AGEs per serving are expressed as kilounits.

Fats	AGEs (U/g)	Serving (g)	AGEs/serving (kU)
Almonds, roasted	66,514	30	1,995
Avocado	15,772	30	473
Butter	264,873	5	1,324
Cashews, roasted	98,082	30	2,942
Cream cheese, Philadelphia soft	108,843	30	3,265
Margarine, 60% vegetable oil	175,192	5	876
Mayonnaise	94,010	5	470
Mayonnaise, imitation	2,000	5	10
Mayonnaise, low fat	22,011	5	110
Olive, ripe	16,686	30	501
Peanut butter, smooth	75,183	30	2,255
Walnuts, roasted	78,874	30	2,366
Salad dressing, Caesar	7,371	15	111
Salad dressing, French, Lite	11	15	0
Salad dressing, Italian, Lite	8	15	0
Beef	AGEs (U/g)	Serving (g)	AGEs/serving (kU)
Frankfurter, boiled 7 min	74,850	90	6,736
Frankfurter, broiled 5 min	112,697	90	10,143
Hamburger, fried 6 min	26,391	90	2,375
Hamburger, fast food	54,176	90	4,876
Meatball, boiled in sauce 1 h	28,519	90	2,567
Meat loaf, crust off, roasted 45 min	18,619	90	1,676
Roast beef	60,708	90	5,464
Shoulder cut, boiled 1 h	22,305	90	2,007
Shoulder cut, broiled 15 min	59,636	90	5,367
Bacon, microwave 3 min	90,228	13	1,173
Deli ham, smoked	23,491	90	2,114
Pork chop, pan fried 7 min	47,526	90	4,277
Beef and pork links, pan fried	54,255	45	2,441
Sausage, pork links, microwave 1 min	59,438	90	5,349
Poultry	AGEs (U/g)	Serving (g)	AGEs/serving (kU)
Chicken breast, skinless cubes, pan fried 15 min	61,221	90	5,510
Steamed 10 min and broiled 12 min	56,348	90	5,071
Pan fried 10 min and boiled 12 min	63,398	90	5,706
Chicken breast, skinless cutlet, raw	7,686	90	692
Boiled 1 h	11,236	90	1,011
Broiled 15 min	58,281	90	5,245
Fried 8 min	73,896	90	6,651
Microwave 5 min	15,245	90	1,372
Chicken breast, with skin, roasted 45 min	60,203	90	5,418
Chicken, dark meat, broiled 1 h	82,992	90	7,469
Chicken loaf, roasted, crust off, 45 min	14,195	90	1,278
Chicken nuggets	86,271	90	7,764
Turkey breast, cubes, skinless, broiled	55,747	90	5,017
Turkey breast steak, skinless, broiled	43,873	90	3,949
Smoked turkey breast, seared	60,137	90	5,412
Fish	AGEs (U/g)	Serving (g)	AGEs/serving (kU)
Fish loaf, boiled 90 min	7,606	90	685
Salmon, breaded, broiled 10 min	14,973	90	1,348
Salmon, raw	5,573	90	502
Salmon, smoked	5,718	90	515
Trout, raw	7,830	90	705
Trout, roasted 25 min	21,383	90	1,924
Tuna, loaf, roasted 40 min	5,895	90 531
Roasted 25 min	9,189	90	827
White, canned in oil, Albacore	17,396	90	1,566
Cheese	AGEs (U/g)	Serving (g)	AGEs/serving (kU)
American, processed	86,775	30	2,603
American, processed, low fat	40,395	30	1,425
Brie	55,979	30	1,679
Cottage cheese 1% fat	14,532	120	1,744
Feta	84,235	30	2,527
Mozzarella, part skim	16,777	30	503
Parmesan, grated	169,020	15	2,535
Swiss, processed	44,701	30	1,341
Eggs	AGEs (U/g)	Serving (g)	AGEs/serving (kU)
Egg yolk, boiled 10 min	12,134	15	182
Boiled 12 min	18,616	15 279
Egg white, boiled 10 min	442	30	13
Boiled 12 min	573	30	17
Egg, fried with margarine	27,494	45	1,237
Tofu	AGEs (U/g)	Serving (g)	AGEs/serving (kU)
Broiled	41,067	90	3,696
Raw	7,875	90	709
Sautéed	38,303	90	3,447
Breads	AGEs (U/g)	Serving (g)	AGEs/serving (kU)
Bagel	1,075	30	32
Greek, hard	1,514	30	45
Whole wheat, center	536	30	16
Whole wheat, center toasted	1,080	30	25
Whole wheat, crust	730	30	22
Whole wheat, crust, toasted	1,394	30	36
Breakfast foods	AGEs (U/g)	Serving (g)	AGEs/serving (kU)
Pancake, frozen, toasted	22,618	30	679
Pancake, homemade	9,722	30	292
Waffle, frozen, toasted	28,711	30	861
Cereals	AGEs (U/g)	Serving (g)	AGEs/serving (kU)
Bran Flakes	346	30	10
Corn Flakes	2,320	30	70
Frosted Flakes	4,270	30	128
Corn Pops	12,431	30	373
Oatmeal instant, dry	188	30	4
Oatmeal, instant with honey	175	175	31
Rice Krispies	19,997	30	600
Grains and legumes	AGEs (U/g)	Serving (g)	AGEs/serving (kU)
Bean, red kidney, raw	1,158	100	116
Bean, red kidney, canned	1,906	100	191
Bean, red kidney, cooked 1 h	2,983	100	298
Pasta, cooked 8 min	1,123	100	112
Pasta, spiral, cooked 12 min	2,420	100	245
White rice, quick cook, 10 min	88	100	9
White rice, converted, cooked 35 min	91	100	9
Starchy vegetables	AGEs (U/g)	Serving (g)	AGEs/serving (kU)
Corn, canned	195	100	20
Sweet potato, roasted, 1 h	723	100	72
White potato, boiled, 25 min	174	100	17
White potato, french fries, homemade	6,939	100	694
White potato, french fries, fast food	15,219	100	1,522
Crackers and snacks	AGEs (U/g)	Serving (g)	AGEs/serving (kU)
Chips, corn, Doritos	5,049	30	151
Lay’s Potato Chips	28,818	30	865
Chips Ahoy Chocolate Chip Cookies	16,837	30	505
Oatmeal raisin cookie	13,707	30	411
Cracker, Goldfish, cheddar	21,760	30	653
Chocolate Chunk Granola Bar	5,068	30	152
Peanut Butter Chocolate Chunk Granola Bar	31,761	30	953
Popcorn with butter, air popped	1,340	30	40
Fruits	AGEs (U/g)	Serving (g)	AGEs/serving (kU)
Apple	127	100	13
Apple, baked	445	100	45
Banana	87	100	9
Cantaloupe	201	100	20
Raisin	201	30	36
Vegetables	AGEs (U/g)	Serving (g)	AGEs/serving (kU)
Broccoli, carrots, celery, grilled	2,260	100	226
Carrots, canned	103	100	10
Green beans, canned	179	100	18
Onion, raw	358	100	36
Tomato, raw	234	100	23
Other carbohydrates	AGEs (U/g)	Serving (g)	AGEs/serving (kU)
Sugar, white	0	5	0
Sugar substitute, powder	58	1	0
Milk and milk products	AGEs (U/mL)	Serving (mL)	AGEs/serving (kU)
Milk, whole	48	250	12
Fat free	5	250	1
Fat free, microwave, 1 min	21	250	5
Fat free, microwave, 3 min	345	250	86
Formula, infant	4,861	30	146
Human milk, fresh	52	30	2
Instant, chocolate, skim milk, sugar free	11	120	1
Yogurt, strawberry or cherry, nonfat, sugar free	40	250	10
Syrups, gels and juices	AGEs (U/mL)	Serving (mL)	AGEs/serving (kU)
Honey	87	15	1
Syrup, caramel, sugar free	15	15	0
Dark corn	14	15	0
Apple	20	250	5
Cranberry	32	250	8
Orange, fresh squeezed	3	250	1
Orange, carton	56	250	14
Dishes	AGEs (U/g)	Serving (g)	AGEs/serving (kU)
Italian pasta salad, homemade	9,346	100	935
Macaroni and cheese, baked	40,698	100	4,070
Pizza, thin crust	68,248	100	6,825
Sandwich, toasted cheese	43,327	100	4,333
Beverages	AGEs (U/mL)	Serving (mL)	AGEs/serving (kU)
Coffee, decaffeinated, instant	53	250	13
Instant	47	250	12
Drip method	15	250	4
On a heating plate more than 1 h	134	250	34
With milk	66	250	17
With milk and sugar	24	250	6
Cola	65	250	16
Cola, sugar free	12	250	3
Tea	19	250	5

Condiments	AGEs (U/mL)	Serving (mL)	AGEs/serving (kU)
Ketchup	103	15	2
Mustard	29	15	0
Soy sauce	573	15	9
Vinegar, balsamic	352	15	5
Vinegar, white	377	15	6

Conclusion Foods high in fat and/or protein are highest in AGEs, while carbohydrates are low in AGEs. The amount of advanced glycation endproducts increases as cooking temperature and time increases. Processed foods in general have more AGEs than unprocessed foods: for example, infant formula milk contains a 100 times more AGEs than human or cow milk. For more information on glycation, see these posts: Yerba Mate Inhibits AGE Formation Green Tea Reduces the Formation of AGEs My Current Health Regimen The 7 Types of Aging Damage That End up Killing You

Selegiline and Lifespan Extension

noreply@blogger.com (JLL) — Sun, 06 Feb 2022 13:20:00 +0000

Deprenyl increases the lifespan of female hamsters. (Photo by MarinaAvila)

Selegiline, also known as deprenyl, is an old life extension drug. It's been around since the 80's, but after some conflicting data from Parkinson's Disease studies, interest in selegiline for life extension purposes has been negligible. These days, deprenyl is mostly used to treat Parkinson's Disease, depression and dementia. Still, the early studies showed such promising results that a review of the studies on deprenyl and longevity is in order. Deprenyl extends maximum lifespan in male rats In the first study on selegiline and lifespan, 24-month old male Wistar-Logan rats were treated subcutaneously with selegiline (0.25 mg/kg) or a saline solution three times a week (link). The control group receiving only saline had an average lifespan of 147 weeks, about 34 months. The longest living rat in this group was 164 weeks (~37 months) old. The deprenyl group did significantly better. In fact, even the shortest living rat receiving selegiline managed to outlive the longest living in the control group, making it to 171 weeks (~39 months). The longest living rat survived for a whopping 226 weeks (~52 months). That's a maximum lifespan increase of 38%. The average lifespan in the deprenyl group was 198 weeks (~46 months). The author, Dr. Joseph Knoll, states:

The average lifespan was higher than the estimated maximum age of death in the rat (182 weeks). This is the first instance that by the aid of a well-aimed medication members of a species lived beyond the known lifespan maximum.

In 1994, Dr. Knoll continued his experiments, again using the same dosing but this time on younger Wistar-Logan rats (28 weeks, or ~6 months old), some of which were sexually inactive and some of which were sexually highly active (link). The sexually inactive control rats remained inactive throughout their life and lived 135 weeks (~31 months), whereas their deprenyl-treated peers suddenly developed a hunger for sex and lived 152 weeks (~35 months), the same as the sexually active control group. The highly active rats given deprenyl became even more sexually active than their saline-treated control group, and lived for 185 weeks (~43 months). Only mean lifespan increases in another strain of rats Between Knoll's experiments on male Wistar-Logan rats, another lifespan experiment on selegiline was done. This time, male Fischer rats were given deprenyl (0.25 mg/kg) or saline subcutaneously every other day, starting at 23 to 25 months of age (link). Again, the deprenyl group lived longer, but this time the effect was not as dramatic as in the previous study. The remaining life expectancy of rats given selegiline was increased by only 16%. Then again, as Ben Best points out in his good summary of deprenyl, Fischer rats live only 28 months, much shorter than Wistar-Logan rats. In 1993, Japanese scientists doubled the standard dose of deprenyl and injected male Fischer rats with 0.5 mg/kg, starting from the age of 18 months (link). The abstract states:

The increases in average life expectancies caused by deprenyl treatment (15% from 18 months and 34% from 24 months) were both statistically significant.

I don't have access to the full paper, so I'm not sure what exactly they mean by this. Were there actually two treated groups, with one given deprenyl since 18 months and the other since 24 months of age, or did the control group start dropping dead faster after 24 months? In any case, maximum lifespan was apparently not increased, unlike in the previous studies. A possible explanation is the shorter lifespan of Fischer rats and the higher dose used. On the other hand, Ben Best says on his website:

At the 2004 American Aging Association Conference Kitani (one of the authors of the Fischer study) reported that he had halved the dose to the standard 0.25mg/kg (3 times per week) and increased mean life span 44% for females and 32% for females starting from 24 months. Nonetheless, no significant increase in maximum lifespan was seen.

If the above is correct, then the higher dose is probably not the culprit. Perhaps treatment has to be begun earlier, or perhaps deprenyl doesn't work in all rat strains. Different doses and forms of deprenyl In 1992, two more studies appeared in a Hungarian journal, with Dr. Knoll as the coauthor in both of them. The first one fed male mice either deprenyl, Dinh lang root extract or a combination of the two three times a week, starting at 12 months of age (link). The abstract states only that the combination was the most potent treatment, increasing both memory function and survival time. The second study used the same dosage of deprenyl as before, but this time 6-month old male Wistar rats and a different form of deprenyl known as (-)p-fluoro-deprenyl were used (link). The study lasted for 25 months. Three of the 20 control rats (15%) and 15 of the 40 deprenyl-treated rats (37.5%) survived until the end. Three of the rats receiving selegiline were still sexually active at 31 months, even though normal male Wistar rats lose their ability to ejaculate by the time they're 2 years old. The authors also experimented with a much smaller dose of selegiline, giving 13-month old non-copulator rats only 0.01 mg/kg instead of the usual 0.25 mg/kg. The lifespan of these rats was short, with the control group living only 102 weeks (~23 months) and the (-)p-fluoro-deprenyl group living 106 weeks (~24 months). Rats given the standard deprenyl lived for 104 weeks. Sexual performance was improved in both deprenyl groups, however. Deprenyl in females, mice, and dogs The first study on selegeline and life extension on female rats came a few years later. Once again, the dosing was 0.25 mg/kg injected three times a week (link). The rats were 6 months old and had their ovaries removed. All the control females were dead before hitting 15 months of age, while all of the deprenyl-treated rats were still alive. Three of them even reached 36 months of age. Unlike in the case of males, however, neither group showed much sexual activity. In Syrian hamsters, a low dose of selegiline increased the lifespan of females but not males, even though MAO-B was inhibited in both groups by the same amount (link). Female controls died younger than male controls, but in the deprenyl group this difference disappeared. Deprenyl seems to increase lifespan also in immunosuppressed mice. When 4 mg of selegiline was mixed in 10 kg of feed, survival improved dramatically (link). The last mouse in the control group died 2.5 months after the study was started, at the age of 5 months, whereas the last mouse in the selegiline group made it to 14.5 months. Deprenyl and dogs Rodents are not the only animals that seem to gain extra years from selegiline. A study on beagle dogs, ranging in age from 2.8 to 16.4 years, studied the effects of orally administered deprenyl on lifespan (link). The dose was 1 mg/kg, four times as high as the one originally used by Dr. Knoll on rats. The study lasted for 2 years and 10 weeks. Almost all of the young dogs survived until the end of the study, but older dogs given deprenyl survived longer than those that were given placebo. 80% of dogs in the deprenyl group survived until the end of the study, compared to only 39% in the placebo group. The first deprenyl-treated dog died on day 247, whereas the first untreated dog died on day 295. Summary In the experiments of Dr. Knoll, who first discovered its life-extending properties, selegiline consistently increased the mean and maximum lifespan of male Wistar-Logan rats. The rats given deprenyl had a maximum lifespan that was up to 38% greater than that of the control rats. The longest living rat in these studies was 52 months old. Only one study looked at female rats and life extension, but it too showed an increased lifespan from deprenyl. Extrapolating directly from rats, the 0.25 mg/kg dose used in the experiments would correspond to 20 mg of selegiline every other day, or 10 mg daily, for a man weighing 80 kg (~176 pounds). For a female weighing 60 kg (~132 pounds), the equivalent would be 7.5 mg daily. Not all of the results have been so uniformly positive, however. While mean lifespan was increased in male Fischer rats, maximum lifespan was not. One possible reason is the shorter average lifespan of Fischer rats, but other explanations cannot be ruled out. Also, male Syrian hamsters given deprenyl did not live longer, although females did. For more information on life extension, see these posts: Does Intermittent Fasting Increase Lifespan? How Do People Feel about Life Extension? Dietary Supplement Increases Lifespan by 11% in Healthy Mice Slowing Down Aging with Intermittent Protein Restriction

How Does Eating Avocados Affect Cholesterol?

noreply@blogger.com (JLL) — Sun, 06 Feb 2022 13:18:00 +0000

Avocados contain plenty of MUFAs, most of which is oleic acid. (Photo by Muffet)

Everyone knows avocados are high in fat, but does that make them healthy or unhealthy? In this post, we'll look at how avocados affect cholesterol levels.

Avocados are technically large berries of the avocado tree, each berry containing a single seed usually called the avocado stone. There are several different cultivars, but on average avocados contain about 15 grams of fat, 9 grams of carbohydrates and 2 grams of protein per 100 grams. Most of the fat (~10 grams) is monounsaturated, while the rest is roughly half saturated and half polyunsaturated.

Most health enthusiasts are either pro-saturated fatty acids (SAs) or pro-polyunsatured fatty acids (PUFAs) – and if you're a long-time reader of this blog, you already know which category I lean towards. Monounsatured fatty acids (MUFAs), however, seem to represent something of a "neutral" group of fats to many. Olive oil, for example, is high in MUFAs, and almost all studies find it either beneficial or at least neutral: generally, LDL decreases and HDL either increases or stays the same.

So if olive oil is good for you, what about avocados? Since both are high in MUFAs, specifically oleic acid, one might expect to see similar results. In rats, adding avocados to their diet seems to increase HDL and decrease triglycerides (link). Avocado leaf extracts appear to be especially effective (link).

Avocados, cholesterol & healthy subjects

Experiments on humans, unfortunately, are not always as unequivocal. The earliest human study I came across find compared an avocado-enriched diet with a diet high in complex carbohydrates and low in fat – namely, the lipid-lowering diet advocated by the American Heart Association (link). The study included 15 women who were randomly assigned to one of the diets for three weeks, followed by 3 weeks on the other diet. Only the avocado diet, on which the women ate between half and one and a half avocados per day, resulted in a statistically significant decrease (~8%) in total cholesterol levels. This was due to a lowering of LDL without affecting HDL, whereas the complex carbohydrate diet lowered HDL levels by ~14%. So much for the heart-healthy effects of low-fat diets.

The second study included 16 healthy volunteers who were fed three different diets for 2 weeks: a high-MUFA diet consisting of 30% fat (75% of which came from avocados), a free diet including avocados, and a low-saturated fat without avocados (link). Both the high-MUFA diet and the low-SA diet reduced total cholesterol and LDL. However, the low-SA diet also also reduced HDL and increased triglycerides, while the other two diets reduced triglycerides. Again, the low-fat diet with an emphasis on limiting saturated fats was the most harmful for cholesterol levels.

I find it somewhat surprising that the free diet with avocados apparently also reduced HDL, even though the authors say the volunteers ate the same amount of avocados as during the high-MUFA diet. Unfortunately I don't have access to the full paper, so I'm not sure what the free diets were like in reality. Perhaps the volunteers simply ate more during the free diet, which could have skewed the results, or maybe the SA/PUFA ratio was significantly lower on the free diet for some reason.

Avocados and people with high cholesterol

Another study included 13 patients with high LDL cholesterol (link). The patients were given a standard vegetarian diet, a vegetarian diet enriched with avocado or a free diet that included avocados. The standard vegetarian diet consisted of 70% carbs, 20% fat and 10% protein, while the vegetarian avocado diet was 60% carbs, 30% fat and 10% protein. The vegetarian avocado diet reduced LDL, whereas the free diet increased it slightly. Only the standard vegetarian diet significantly reduced triglycerides – however, it also reduced HDL more than the other two.

The results of this study seem to contradict the two earlier studies, since simply adding avocados to the diet resulted in slightly lower HDL and slightly higher LDL – in other words, their cholesterol levels worsened. Genetics may play a role here, as some individuals who are predisposed to higher LDL levels seem to react negatively to foods that generally improve the cholesterol ratio. The authors themselves state:

"Low-fat, carbohydrate-rich vegetarian diets may be harmful to hypercholesterolemic patients. The avocado addition to a vegetarian diet does not correct these undesirable effects. To obtain beneficial effects on lipid profile with avocado, lower amounts of carbohydrates and polyunsaturated fatty acids are probably needed."

Yet another study compared the effect of an avocado-enriched diet on healthy subjects and patients with slightly elevated cholesterol levels (link). In healthy participants, total cholesterol decreased by 16% on the avocado diet. In participants with high cholesterol, total cholesterol decreased similarly, with LDL and triglycerides decreasing by 22% and HDL increasing by 11%. The authors conclude that a high-MUFA diet containing avocados improves lipid profile in healthy and especially in mildly hypercholesterolemic people.

Conclusion

Compared to low-fat diets, diets containing moderate to high amounts of monounsaturated fatty acids from avocados seem to result in better cholesterol levels. In healthy people, replacing carbohydrates with avocados generally lowers LDL without affecting HDL, similar to olive oil. In people with high cholesterol, replacing carbohydrates with avocados appears to reduce LDL and, in some cases, increase HDL.

The controversial result is the lower HDL in free diets with avocados. Does simply adding an avocado to your diet actually make cholesterol levels worse? This is a tricky question, since adding an avocado would mean an increase in total energy intake, unless it also means you eat less of something else – which would be the case, unless avocados somehow increase appetite. One possibility is that when the participants added avocados (and thus MUFAs) to their diet, they reduced their consumption of other fatty acids while keeping total energy intake the same. Reducing saturated fatty acid intake could result in lower HDL, although this doesn't necessarily explain the higher LDL. Without knowing what the participants actually ate during their free diet periods, it's difficult to say what the cause is.

While it's generally taken for granted that a) olive oil reduces LDL and has a neutral or positive effect on HDL and b) this effect is due to the high MUFA content of olive oil, there are differences in the food sources of MUFAs. Both avocados and olive oil are high in oleic acid, but olive oil contains squalene, whereas avocados do not. Squalene is a precursor in cholesterol synthesis and is metabolized to cholesterol in the body. Avocados, on the other hand, contain beta-sitosterol, which lowers LDL.

Finally, genes play a major role in cholesterol levels. Apolipoprotein E genotype affects how individuals react to dietary fatty acids and also cholesterol-lowering drugs like statins. Without knowing the genotypes of the participants in the studies, it's hard to say how generalizable the results are.

For more information on diet and cholesterol, see these posts:

Want to Increase Your HDL Cholesterol by 50%? Sage Tea May Be the Answer
High HDL Cholesterol Reduces Risk of Dying in Men
Hibiscus Tea Increases HDL, Lowers LDL and Triglycerides
The Twinkie Diet: Thoughts on Weight Loss and Cholesterol

Rinsing with Green Tea Improves Oral Health

noreply@blogger.com (JLL) — Sun, 06 Feb 2022 13:11:00 +0000

Rinse with green tea and keep your teeth happy. (Photo by Daria)

I've written before about the protective effects of green tea against dental caries. Several studies have shown that green tea helps tooth and gum health by reducing harmful bacteria, increasing enamel strength and inhibiting the breakdown of starch to sugar.

Black tea, cocoa and coffee protect against oral problems too, but green tea seems to be the most effective. A new study sheds more light on how drinking green tea improve oral defense mechanisms through oral peroxidases (OPOs) (link).

The two major defensive peroxidases of the mouth are salivary peroxidase (SPO) and myeloperoxidase (MPO). Their function depends partly on diet and probably also on genes.
In the abstract, the authors mention that their earlier study showed that elderly people who drank green tea for 3 months had higher levels of oral peroxidase activity than non-drinkers. In this study, they compared the effects of green tea on OPO in vivo and in vitro.

Adding a green tea infusion to saliva increased oral peroxidase activity by 280%, while black tea increased it by only 54%. Adding only epigallocatechin gallate (EGCG), the main polyphenol in green tea, increased activity by 42%. The effect was dose-dependent, which I assume here means that the stronger the tea, the greater the effect.

In human subjects, green tea gave a very similar result. Mouth rinsing with a green tea infusion resulted in a 268% increase in OPO activity. Thus, while green tea extracts may be more useful than just drinking regular green tea for some purposes, for dental health drinking and/or rinsing is probably the most effective way.

Note, however, that higher levels of salivary peroxidase don't necessarily mean better oral health; in fact, people with more dental caries and gingivitis tend to have higher SPO activity (link). My guess is that this is a defense mechanism against the harmful effects of excess hydrogen peroxide, which is excreted by oral bacteria. In other words, the stronger the attack, the stronger the defense.

In the case of green tea it seems that increasing SPO really does lead to better oral health, though.

For more information on green tea and dental health, see these posts:

Drinking 10 Cups of Green Tea Daily and Not Smoking Could Add 12 Years to Your Life
Green Tea Extract Enhances Abdominal Fat Loss from Exercise
Vegetable vs. Animal Sources of Vitamin A: Why Eating Carrots Isn't Enough
Genes, Diet and Oral Health: Why Do Some People Get Cavities and Others Don't?

Antioxidants and Intermittent Fasting – Good For Longevity?

noreply@blogger.com (JLL) — Thu, 15 Mar 2012 18:42:00 +0000

Are blueberry antioxidants beneficial for intermittent fasting? (Photo by Simply Bike)

Is it possible to live longer by combining the benefits of intermittent fasting (IF) and plant polyphenols? A new paper claims that taking polyphenol antioxidants during dietary restriction increases the lifespan of mice more than dietary restriction alone. The antioxidants used in the study were blueberry, pomegranate and green tea extracts.

The subject of the paper – "Potentiation of dietary restriction-induced lifespan extension by polyphenols" – is certainly enough grab the attention of anyone interested in life extension. The abstract seems promising too (link). Here's a quote:

Dietary restriction (DR) extends lifespan across multiple species including mouse. Antioxidant plant extracts rich in polyphenols have also been shown to increase lifespan. We hypothesized that polyphenols might potentiate DR-induced lifespan extension. [––] Polyphenol compounds may potentiate IF-induced longevity by minimizing specific components of IF-induced cell stress.

Let's look at these claims in more detail. First off, it's not clear from the abstract what exactly the authors mean by "dietary restriction". The full paper, however, reveals that they use the term to describe pretty much any kind of diet where access to food is limited, including traditional calorie restriction and intermittent fasting.

The longevity confusion

The problem with that opening sentence is that dietary restriction extends lifespan across multiple species only when it equals calorie restriction. That is, you can make a mouse live longer by only feeding every other day, as long as it results in less calories consumed. This is an important distinction, because many people – including longevity scientists – keep propagating the myth that intermittent fasting has the same benefits as calorie restriction. It doesn't. The reason that IF prolongs lifespan in some species is because the animals fail to compensate for the missed calories on their feeding days.

The next sentence is just as problematic. Yes, plant antioxidants have been shown to increase lifespan, but the question is, compared to what? So far, no one has succeeded in exceeding the known maximum lifespan of mice by feeding them antioxidants. Instead, what we see in many studies is that the antioxidant group lives longer than the control group.

The problem is that almost always, neither group lives very long. Poor diets, poor animal husbandry, poor environment – all play a role in how long the animals live. So, in essence, the antioxidants merely make the unhealthy mice a bit healthier. But this is like making a human live 70 years instead of 60 years by giving them some veggies with his daily bread and then claiming that "vegetables extend human lifespan".

Comparing lifespans

That said, there are some interesting figures in the full paper. The graph below shows the survival rates of the three groups; one fed the control diet, the second fed the same diet but only every other day, and the third fed a diet supplemented with polyphenols every other day:

There's a big drop in the survival rate of the control group around 22 months. For the IF groups, the survival curves look a lot better. So how does this compare to the average lifespan of similar mice kept in good laboratory conditions? Here's a graph of age ranges and survivorship of C57BL7/6J mice (the same strain used in this study):

This survival curve is based on a cohort of 150 male and 150 female mice. As you can see, at 28 months half of the mice are still alive. That's about 850 days, which is a pretty normal figure for mean lifespan of this strain of mice in the literature.

Once again, in the antioxidant study the control group dies earlier than is normal. For some reason, half of the mice are dead at 22 months instead of 28 months. One possible reason is the use of a high-fat diet to "mimic the effects of a Western diet", as the authors put it. This seems like a strange idea to me, because a typical Western diet is no more a high-fat diet than it is a high-carbohydrate diet. Furthermore, plenty of humans (myself included) seem to do quite well on a high-fat diet, whereas with mice it's somewhat different.

The survival curve of the IF mice in the first graph is slightly better than that of the normal-fed mice in the second graph. But that is hardly a surprise, given that both the IF group and the IF + antioxidant group had lower body weights than the control group. In other words, the intermittent fasting once again made the mice eat less than the control group, which in turn resulted in a slightly longer lifespan. It's good to keep in mind, however, that with just 10% calorie restriction longer lifespans have been reported in other studies, so the result is not too impressive.

Conclusion

Perhaps the most interesting result is that the IF + antioxidant group lived slightly longer than the IF group. There's no concensus as to whether it's a good idea to combine CR or IF with antioxidants. It may be that plant polyphenols are essential for optimal nutrition and good for activating sirtuins (which play at least some role in longevity), but there is also some evidence suggests that taking antioxidants may interfere with hormesis and thus diminish the effects of CR.

In this study, the antioxidants had a beneficial effect. While the IF diet by itself activated pro-inflammatory pathways, adding plant polyphenols to the diet blocked this effect. The authors identified 20 gene sets that were down-regulated by the addition of polyphenols, most of them related to immune response, inflammation, cell differentation and tumorigenesis.

This suggests that if you're doing intermittent fasting, adding some blueberries, pomegranates and green tea to your diet may not be such a bad idea. Note, however, than the mice did not have access to polyphenols during their fasting days, so this study tells us nothing about taking antioxidants during fasting. It also doesn't say much about how polyphenols affect regular calorie restriction without IF in humans.

For more information on intermittent fasting and longevity, see these posts:

Lithium in Drinking Water May Lead to Longer Life
Does Intermittent Fasting Increase Lifespan?
Alternate-Day Feeding and Weight Loss: Is It the Calories Or the Fasting?
Slowing Down Aging with Intermittent Protein Restriction

Guest Post: Natural Alternatives for Arthritis Treatment

noreply@blogger.com (JLL) — Mon, 07 Nov 2011 11:15:00 +0000

Glucosamine is also found in seashells. (Photo by DavidRPhoto)

Guest post by Emily Matthews

Glucosamine sulfate and chondroitin sulfate have long been used as supplements to ease the pain of arthritis. Both compounds are found naturally in animal cartilage and glucosamine can also be found in seashells. A person who wishes to increase the amount of glucosamine and chondroitin in their diet should take them together as supplements, but only from a reputable manufacturer of vitamins and supplements. Medical professionals are uncertain as to the dosage for the average person.

Chondroitin

Chondroitin is a more complex molecule than glucosamine. It's made up of intact or hydrolyzed glycosaminoglycans with attached sugar molecules. Studies from masters degree programs show that it’s not as effective as glucosamine in treating arthritis, as the body doesn’t absorb as much of it; chondroitin is such a large molecule that it's difficult to pass through the normal intestinal barrier. The benefit of chondroitin comes because at least some of it can be broken down into glucosamine in the digestive track.

Glucosamine

Glucosamine is a simple molecule made up of glucose and an amine, which is a building lock of protein. The main effect of glucosamine is to stimulate the creation of glycosaminoglycans, which helps cartilage remain spongelike and act as a cushion between joints. As some people age, their bodies lose the ability to manufacture glucosamine and so the cushioning effect of cartilage is lost. Some studies claim that glucosamine supplements are more effective than placebos or non-steroidal anti-inflammatory drugs in easing arthritis pain

GAIT Trials

In a recent study, the National Center for Complementary and Alternative Medicine conducted the Glucosamine Chondroitin Arthritis Intervention Trial, or GAIT to see if glucosamine and chondroitin sulfate gave any benefits in the treatment of arthritis of the knee. The study was conducted to see if the supplements, used alone or separately, eased the pain of 1583 sufferers of this form of arthritis.

In GAIT, the people who participated in the double blind trial took glucosamine alone, chondroitin sulfate alone, the two supplements together, the prescription drug celecoxib, or a placebo. The results of the trial were that celecoxib significantly reduced the pain of knee arthritis and that glucosamine and chondroitin, taken alone or separately, were no better than the placebo in reducing pain. However, there was a small group of participants with what they described as "moderate to severe pain" who found that the glucosamine and chondroitin sulfate combination reduced their pain significantly.

The efficacy of glucosamine and chondroitin in treating arthritis is uncertain. Glucosamine seems to provide some relief for some arthritis sufferers. Chondroitin is too large a molecule to be absorbed by the body in any appreciable amount. If the glucosamine and chondroitin combination works for some people, it’s probably because enough chondroitin is broken down to increase the effect of the glucosamine.

Emily Matthews is currently applying to masters degree programs across the U.S., and loves to read about new research into health care, gender issues, and literature. She lives and writes in Seattle, Washington.

For more information on glucosamine, chondroitin and arthritis, see these posts:

Green Tea Protects Cartilage from Arthritis in Vitro
Green Tea Protects from Arthritis in Rats
MSM + Chondroitin + Glucosamine for Hair & Nail Growth - Results after Seven Weeks
MSM + Chondroitin + Glucosamine: A Sulfur Cocktail for Hair and Nails

Topical vs. Oral Antioxidants for Sun Protection – Which Is Better?

noreply@blogger.com (JLL) — Mon, 19 Sep 2011 14:54:00 +0000

Eating the right foods can protect your skin from the sun. (Photo by Extra Medium)

While studies on antioxidants are generally pretty disappointing when it comes to life extension, they do have some use as anti-aging treatments for the skin.

While all or most antioxidants appear to protect from the harmful effects of the sun, some antioxidants are more effective than others. Carotenoids are a case in point. One example is lycopene, which is found in tomatoes. For example, one study showed that people who ate tomato paste daily had 33% more protection against sunburn compared to the control group.

Among carotenoids, lutein seems to give the best bang for the buck. In addition to photo-protection, lutein increases skin hydration and lipid levels while reducing lipid peroxidation.

But is it better to use antioxidants topically or orally? Some folks swear by their skin creams, while others maintain that eating the right foods is the best way to improve the skin. In the lutein study, the combination of taking a lutein supplement and using a lutein cream gave the best results. Not all that surprising – by using topical and oral treatments you're covering both grounds and playing it safe, after all.

However, a recent paper got me thinking whether "attacking the problem from all angles" is really the best way to go at it. The study looked at carotenoid levels in the skin after using carotenoids topically and systemically (link). 129 healthy women, aged between 21 and 72 years, were divided into seven different groups and given topical creams, oral supplements, both, or a placebo.

The first cream contained a basic mixture of antioxidants from sources such as vitamin E, vitamin C and green tea. The second cream contained the same antioxidant mix complemented by beta-carotene and lycopene. Similarly, the first supplement contained antioxidants from sources like green tea, green coffee, and pongamia pinnata seeds, while the second also contained carotenoids.

The placebo treatments did not increase carotenoid concentration in the skin, while the carotenoid cream increased it by 30% in the forehead and 35% in the cheek. That's not bad – until you look at the results in those subjects who used the tablets instead. Taking the antioxidant supplement containing carotenoids resulted in an 80% increase in the forehead and 70% in the cheek after just four weeks.

The interesting part is the group who used both the cream and the supplements. After four weeks, the results were similar to the group using only the supplement, with the supplement-only group actually scoring better in some areas. After eight weeks the group using both treatments saw the best results.

However, whereas the effect from using the cream lasted for only 10 days after stopping treatment, the results from taking the supplement were sustained for up to 5 weeks. The authors also point out that "surprisingly, the combined application of both tablets and creams containing carotenoids did not reach the satisfying result obtained with the application of tablets only".

The result is indeed unexpected, since using the antioxidant + carotenoid cream along with the antioxidant + carotenoid supplement did in fact yield the largest carotenoid concentration. However, using the antioxidant + no carotenoids cream together with the antioxidant + carotenoid supplement gave worse results than skipping the cream altogether. That is, using the cream somehow negated some of the benefits of the supplement.

According to the authors, it's possible that systemically applied antioxidants are absorbed and transported onto the skin surface with sweat and sebum and that applying a cream won't increase the concentration any further. This is because the strateum corneum, the outermost layer of the epidermis, acts as a reservoir for topically applied substances.

Hence, when you apply a skin cream, it penetrates into this layer and saturates the reservoir, which makes it impossible for systemically absorbed antioxidants to penetrate into the same layer through sweat and sebum. The authors state that compared to taking only an oral supplement, taking a supplement and applying a cream results in a lower carotenoid concentration.

To avoid this problem, the authors suggest that the formulation of the topical cream should be such that it does not saturate the reservoir and prevent the oral antioxidants from being transported into the skin. In effect, they advise against using lipid-rich formulations.

Many people seem to have seen good results in photo-protection from using oral supplements only. While combining it with topical creams may potentially give the optimal result, this study suggests that finding the right kind of product is important.

For more information on skin care, see these posts:

Tretinoin Results After a Year – Experiment Update
BioSil, JarroSil & Beer – Silicon Experiment Conclusion
Topical Vitamin C for Skin: Re-examining the Case
How to Get Natural Sun Protection by Eating the Right Foods

Kudzu Is an Anti-Androgen and Hair Growth Promoter

noreply@blogger.com (JLL) — Tue, 16 Aug 2011 15:55:00 +0000

Kudzu will grow over anything in its path. (Photo by jjjj56cp)

In traditional Chinese Medicine, kudzu – a quick-growing vine native to China and Japan – is commonly used to treat alcoholism and hangover. This may be due to its potential to increase blood levels of alcohol when taken with an alcoholic beverage. Indeed, at least one study found that giving kudzu to heavy drinkers resulted in lower alcohol consumption (link).

The name kudzu encompasses at least five different species of the plant genus Pueraria. While all of them have very similar properties and are can be used for their medicinal purposes, the most often mentioned species are Pueraria lobata and Pueraria thomsonii. The various species contain a significant amount of isoflavones, which may at least partly be behind their use as a treatment for alcoholism.

Isoflavones, however, also have other uses. Because of their slight estrogenic effect, isoflavones from sources such as soy have been studied as a cure for hair loss. The idea is that isoflavones can inhibit 5-alpha-reductase, which converts testosterone into DHT. Since DHT binds to androgen receptors more potently than testosterone, DHT is a major cause of hair loss in genetically predisposed individuals.

Although the root part of the plant is often used, a recent study showed that the flowers of Pueraria thomsonii were much more effective in inhibiting 5-alpha-reductase than the roots of Pueraria lobata (~51% vs. ~7%). The flowers were powdered and made into a 50% ethanol extract, which was then applied onto the backs of mice after a testosterone treatment (link).

Applying the flower extract improved hair growth in a dose-dependent manner. The mice that got the largest dose (5 mg/day) after testosterone had a hair growth score similar to the control mice that were not treated with testosterone. In other words, the kudzu treatment reversed almost all of the hair loss effects of testosterone.

The authors also applied the extract on C3H/He mice without the testosterone to see whether it would promote hair growth independently of an anti-androgenic effect. The higher dose was almost as effective as minoxidil in promoting hair growth. Although the mechanism was not clear, the authors note that the flowers have been shown to have an angiogenetic effect.

Like soy, kudzu contains significant amounts of the isoflavone daidzein, daidzin and genistein. However, kudzu also contains an isoflavone called puerarin, which is not found in soy. Furthermore, Pueraria thomsonii flowers contain both soyasapones (one of the main components of soy beans) and kaikasaponins (not found in soy), making it rather unique.

I've seen a couple of soaps and shampoos that list kudzu as an ingredient, but I doubt that the amounts are large enough to truly make a difference. If you want to try kudzu topically, you might have better luck buying an extract in powder form and making your own topical. Another possibility is simply taking it orally. There is, after all, evidence that dietary isoflavones promote hair growth.

For more information on hair growth, see these posts:

Biotin Goes Back on the Menu
Soy Isoflavones and Chili Pepper for Hair Growth – Experiment Update
Topical Retinoids Increase Hair Growth in Most People
Zinc Pyrithione Reduces Shedding and Moderately Promotes Hair Growth

Green Tea Polyphenol Heals Stomach Ulcers

noreply@blogger.com (JLL) — Thu, 26 May 2011 08:43:00 +0000

Green tea is a good candidate for treating stomach ulcers. (Photo by toughkidcst)

Non-steroidal anti-inflammatory drugs (NSAID) are generally used for treating pain and reducing fever. The most common NSAIDs are aspirin and ibuprofen. While effective, these drugs have some pretty nasty side effects. For example, up to one in four regular users develop a chronic gastric ulcer at some point.

In addition to causing gastric, peptic and duodenal ulcers, NSAIDs also delay ulcer healing. In the United States, upper gastrointestinal problems from non-steroidal anti-inflammatory drug use result in 16,500 deaths every year. What's worse, almost half of the prescriptions for NSAIDs are estimated to be unnecessary. Anti-ulcer drugs, on the other hand, are expensive and do not prevent the ulcers from recurring.

In a recent Indian study, the effectiveness of the anti-ulcer drug omeprazole and one of green tea's polyphenols, epigallocatechin gallate (EGCG), was compared in mice (link). The mice were first given enough of a NSAID called indomethacin to cause stomach ulceration. After that they were split into three groups: the first group was given a standard effective dose of omeprazole (3 mg/kg), while the second group was given EGCG in various doses (0.5–5 mg/kg). The third group acted as the control group and was given no treatment.

After three days, the ulcers of the mice in the control group had not healed at all. The omeprazole-treated mice had healed ~75% of their stomach ulcers. The effectiveness of the green tea polyphenol was dose-dependent: with 3 mg/kg, the ulcers healed as effectively as with omeprazole, while the largest dose (5 mg/kg) resulted in ~82% healing.

Non-steroidal anti-inflammatory drugs cause gastric ulcers through a variety of mechanisms. They increase the production of reactive oxygen species (ROS), increase lipid peroxidation and cause an imbalance in cytokines which regulate the immune system. In this study, EGCG improved all three factors even more effectively than omeprazole.

Although both omeprazole and epigallocatechin gallate have antioxidant properties, the mechanisms through which they work differ from each other. The main reason omeprazole works is because it reduces the production of gastric acid, whereas green tea is said to increase gastric acid release. While more studies are probably needed, the authors of the paper consider EGCG a promising candidate for treating stomach ulcers because it has not been shown to have negative side effects even with large doses (although there are potential problems with high-dose green tea extracts).

For more information on green tea, see these posts:

Green Tea Protects from the Psychological Effects of Stress in Rats
Tea, Coffee and Cocoa: All Good for Your Teeth
Green Tea and Capsaicin Reduce Hunger and Calorie Intake
Green Tea Extract Increases Insulin Sensitivity & Fat Burning during Exercise

Lithium in Drinking Water May Lead to Longer Life

noreply@blogger.com (JLL) — Wed, 11 May 2011 10:16:00 +0000

Water may have an effect on your longevity. (Photo by anthony_goto)

Lithium is an essential trace element found mostly in drinking water and vegetables. However, nutritional intake of lithium varies considerably, depending on where you live.

In rats, a deficiency of lithium causes health problems such as behavioral abnormalities, but in humans, lithium deficiency is an unknown concept. On the other hand, there have been studies suggesting that lithium intake, even at low doses, is inversely correlated with suicide risk. High-dose lithium has been used for decades to treat psychiatric conditions such as bipolar disorder.

Lithium may also have other life-extending properties besides reducing suicide risk. For example, roundworms have been shown to live up to 36% longer when given lithium chloride, but the amounts used are 1000-fold higher than would be obtainable through diet. Such a high dose may not be necessary, however. In a recent paper roundworms were shown to live longer when given a low concentration of lithium chloride throughout their life – with the effect being less pronounced than with high doses (link).

The authors also looked at lithium in drinking water and total mortality in 18 neighboring Japanese municipalities. They found that tap water levels of lithium were inversely associated with overall mortality adjusted for age and gender. Since lithium levels have been associated with lower suicide rates, the authors also adjusted for suicide. The inverse association between lithium and overall mortality remained.

Lithium concentrations in drinking water ranged from 0.7 to 59 mcg/L. The highest value equals a concentration of 8.5 micromoles. A lithium concentration of 10 micromoles was enough to extend the lifespan of roundworms, while a concetration of 1 micromole was not.

The inverse association between mortality and lithium in drinking water obviously does not prove that lithium reduces mortality in humans, but the roundworm experiments show that the idea is not so far-fetched. Although the mechanism is still unknown, I wonder if the mental health aspect has something to do with it.

Too bad there doesn't appear to be any lithium in the tap water where I live, or at least they don't report it. It is also available as a supplement, but some countries may have customs restrictions on some or all forms lithium.

For more information on longevity, see these posts:

High HDL Cholesterol Reduces Risk of Dying in Men
Selegiline and Lifespan Extension
Does Intermittent Fasting Increase Lifespan?
The 7 Types of Aging Damage That End up Killing You

Drinking Coffee = Higher Adiponectin = Lower Body Fat Percentage?

noreply@blogger.com (JLL) — Thu, 05 May 2011 12:49:00 +0000

Want to lower your body fat? Coffee might an option. (Photo by annais)

Adiponectin is a protein hormone that modulates several metabolic processes related to weight gain. Adiponectin levels are inversely correlated with body fat percentage (link) – for example, diabetics have lower levels of adiponectin than non-diabetics, and losing weight increases adiponectin levels.

Since adiponectin affects glucose uptake and insulin sensitivity, and low adiponectin levels are a risk factor for developing diabetes and metabolic syndrome, it raises the question of whether increasing adiponectin levels might be a good thing.

A study from last year looked at the effects of coffee on adiponectin levels in 665 Japanese males (link). Adiponectin levels were measured from serum samples, and coffee consumption was assessed using a self-administered questionnaire. The questionnaire also included green tea consumption, so that the effects of green tea and coffee could be compared.

The participants who drank more coffee tended to be younger, more likely to smoke, and less likely to drink alcohol. The mean age of non-drinkers was 49.9, while the mean age of those who drank at least three cups per day was 48.2. Interestingly, non-drinkers had the highest mean blood pressure (systolic 129.5 and diastolic 80.7 mmHg) of all groups, while those who drank 1-2 cups per day had the lowest (123.1 and 76.7) – although this could just be due to the age difference. There were no significant differences in BMI or physical activity between coffee drinkers and non-drinkers. Unfortunately, body fat percentage was not measured.

However, adiponectin levels were significantly higher in those who drank coffee compared to non-drinkers. In those who drank none, 1–5 cups per week, 1–2 cups per day, and >2 cups per day, adiponectin levels were 5.95, 6.51, 7.05 and 6.89 mcg/mL, respectively.

When confounding factors such as age, smoking status and BMI were adjusted for, adiponectin levels were still positively associated with coffee consumption. There was a significant dose-response relationship between coffee consumption and adiponectin levels. However, there were no significant differences in adiponectin levels between those who drank 1–2 cups and those who drank >2 cups per day.

Green tea was not associated with adiponectin levels. There was also no association between coffee consumption and total cholesterol, HDL or LDL.

Although this study included only men, similar findings have been reported in women. In one study, diabetic and non-diabetic women who drank at least four cups of coffee per day had higher adiponectin levels than those who didn't drink coffee regularly (link). Interestingly, caffeine consumption was also associated with adiponectin levels. Perhaps the adiponectin-increasing effect of caffeine is diminished or blocked by other compounds such as L-theanine in green tea.

There's also one interventional study on habitual coffee drinkers that found coffee consumption increased adiponectin levels (link). Unlike in the study on Japanese males, total cholesterol and HDL also increased – possibly because the intake of coffee was higher (8 cups per day) at the end of the experiment.

Based on this and other studies, the key points are:

a) those who drink coffee have higher adiponectin levels than those who don't
b) those who have higher adiponectin levels have lower body fat percentage

All in all, while correlation does not prove causation, it seems plausible that drinking coffee could help maintain a lower body fat percentage and avoid type II diabetes and metabolic syndrome.

If you have personal experiences with coffee and weight loss, feel free to share them in the comment section below. For more information on weight and fat loss, see these posts:

Why Are Thin People Not Fat?
A Year of Intermittent Fasting: ADF, Condensed Eating Window, Weight Loss, And More
Green Tea and Capsaicin Reduce Hunger and Calorie Intake
The Twinkie Diet: Thoughts on Weight Loss and Cholesterol

Want to Increase Your HDL Cholesterol by 50%? Sage Tea May Be the Answer

noreply@blogger.com (JLL) — Thu, 28 Apr 2011 13:00:00 +0000

Common sage tea increases HDL and reduces LDL. (Photo by Kelly Johnson)

Salvia officinalis, also known as common sage or garden sage, has been used for hundreds of years both for cooking and healing purposes. It's the variety you can find in most grocery stores – not to be confused with the psychoactive herb Salvia divinorum.

While you might not get hallucinations from common sage, it does have a wide range of health benefits. For instance, sage is commonly used for its antibiotic and antispasmodic properties. In medieval times, sage was generally associated with longevity.

One less well known use for common sage is cholesterol. Nonetheless, a 2009 pilot trial with six healthy female volunteers (aged 40–50) looked at how drinking sage tea would affect their blood glucose regulation and lipid profiles (link). They also evaluated the antioxidant properties of sage tea.

To prepare the tea, 300 mL of boiling water was poured over 4 grams of dried Salvia officinalis plant material and allowed to steep for 5 minutes. Each participant drank the tea twice a day for four weeks.

The graphs above show total cholesterol (A) and HDL cholesterol levels (B) of the participants at baseline (white bar), after two weeks, after four weeks (grey bars) and after a two-week washout period (black bar).

While total cholesterol decreased only marginally after two and four weeks of drinking sage tea, there was a 16% drop in total cholesterol two weeks after the treatment ended. HDL cholesterol, on the other hand, increased after just two weeks. After four weeks, HDL levels were up by ~50%. Two weeks later, they were still ~38% higher than at baseline.

The graphs above show the LDL cholesterol levels and LDL/HDL ratios of the participants. There was a gradual reduction in LDL levels during and after treatment, with a ~20% drop seen after the two-week washout period. Consequently, the LDL/HDL ratio improved throughout the four weeks and remained significantly better after the washout period compared to baseline.

Although the sample size is very small, and this was a non-randomized crossover trial, the figures look very promising. I mean, a 50% increase in HDL in just four weeks? Where else are you going to see improvements like that in healthy people?

The authors also evaluated the antioxidant properties of sage tea by measuring erythrocyte antioxidant status. Both superoxide dismutase (SOD) and catalase (CAT) activity increased significantly after two weeks. Unlike the effect on cholesterol levels, however, there was no significant difference after four weeks compared to baseline. It would be interesting to see a comparison between drinking sage tea daily and cycling it. Who knows, maybe something like two weeks on, two weeks off would be better than drinking it constantly.

Although it has been suggested that sage improves glucose tolerance and insulin sensitivity, the results of oral glucose tolerance tests did not change after four weeks of drinking sage tea. While the participants were healthy, they did belong to a risk group for developing pre-diabetes based on their age. It may be that sage is helpful in those who are already pre-diabetic or diabetic but not in healthy people. On the other hand, the expression of the heat shock protein Hsp70, which is involved in insulin sensitivity, increased by 2.8-fold in lymphocytes after two weeks and remained elevated after the washout period.

For more information on improving HDL and reducing LDL, see these posts:

Hibiscus Tea Increases HDL, Lowers LDL and Triglycerides
Anthocyanins from Berries Increase HDL and Lower LDL
Low-Carb vs. Low-Fat: Effects on Weight Loss and Cholesterol in Overweight Men
Niacin Raises HDL, Lowers LDL, VLDL & Triglycerides

High HDL Cholesterol Reduces Risk of Dying in Men

noreply@blogger.com (JLL) — Wed, 20 Apr 2011 11:49:00 +0000

Strawberry margarita – the perfect longevity drink. (Photo by bookgrl)

According to conventional wisdom, LDL is the "bad cholesterol" and HDL is the "good cholesterol". While there is plenty of evidence showing this is an oversimplification, it is generally agreed that the higher your HDL is, the better. In fact, I've never seen anyone suggest a "maximum" HDL level for a healthy person.

One of the many strange things you hear most doctors recommend is that you reduce your total cholesterol once it's above a certain level, despite what your LDL and HDL are. That is, even if HDL makes up most of your total cholesterol, you may still get a warning that your total cholesterol is "too high". But why would you want to reduce your HDL cholesterol?

High HDL is generally believed to be associated with longevity, at least to a degree. For example, centenarians and supercentenarians tend to have higher HDL than the general population. To my knowledge, large population studies on HDL and longevity are relatively rare, however – which is why I found this new paper from the American Journal of Cardiology pretty interesting (link).

The study (which began in 1979) looked at the probability of 652 men, aged 65 years, to reach 85 years of age. The authors hypothesized that men with higher HDL cholesterol levels in middle age would be less likely to die before 85 years of age than men with lower HDL levels.

For the analysis, participants were categorized into three groups based on their HDL cholesterol: <40, 40–50 and >50 mg/dL. Converted to mmol/L, the ranges are <1, 1–1.3 and >1.3 mmol/L. To me, these categories seem like they're in the lower range of the healthy spectrum, but then again, average HDL levels in men in the US are said to be 40-50 mg/dL. According to the American Medical Association, less than 40 mg/dL is undesirable and higher than 60 mg/dL is desirable.

The age-adjusted hazard ratios for death before 85 years of age in the three groups were as follows: 1.00 for those with HDL < 40 mg/dL, 0.99 for those with HDL between 40–50 mg/dL, and 0.77 in those with HDL > 50 mg/dL. In the fully adjusted model (which accounted for age, LDL, hypertension, smoking, BMI, etc), the hazard ratios were 1.00, 1.01 and 0.72, respectively. That is, men with HDL higher than 50 mg/dL had a ~28% lower risk of dying than those with HDL lower than 50 mg/dL.

Immediately we can see that it doesn't make much difference whether the participants' HDL was below 40 or between 40 and 50 mg/dL – the risk of dying before 85 years of age was pretty much the same for both groups. Only once their HDL cholesterol levels were above 50 mg/dL was there a significantly lower risk.

Furthermore, when the authors analyzed the data further, they found that each 10-mg/dL increment in HDL cholesterol was associated with a 14% decrease in risk of dying before 85 years of age. In other words, the higher their HDL, the higher the survival rate.

This is all very good news. Reaching a HDL level of, say, 80 mg/dL (~2.1 mmol/L) is not at all impossible as long as you plan your diet properly, and would give you a significantly lower risk of dying from cardiovascular disease – which is the number one killer in the 65–85 age group.

The baseline characteristics of the participants reveal some interesting things too. First, the LDL cholesterol was pretty much the same in all groups: around 160–168 mg/dL. Body mass index, on the other hand, was inversely correlated with HDL levels: those with the lowest HDL levels had a mean BMI of 27.5, while those with the highest HDL levels had a mean BMI of 25.8.

While alcohol is known to increase triglycerides in the short term, it also increases HDL. Indeed, alcohol consumption was positively correlated with HDL levels. The percentage of participants who drank at least 2 alcoholic beverages per day was ~14% in those with the lowest HDL, ~18% in those with average HDL and ~38% in those with the highest HDL. This might explain, in part, why moderate alcohol consumption is associated with increased longevity.

So, if your total cholesterol is high and it's mostly due to high LDL, that may be a potential cause for worry – although it's good to keep in mind that there are several types of LDL, some more harmful than others. However, if you have high cholesterol due to high HDL, well then you should be happy!

For more information on HDL cholesterol and how to increase it, see these posts:

Hibiscus Tea Increases HDL, Lowers LDL and Triglycerides
Refined vs Red Palm Oil and Cholesterol
What a "Heart-Healthy" Diet Does to Your Cholesterol Levels
Anthocyanins from Berries Increase HDL and Lower LDL

Biotin Goes Back on the Menu

noreply@blogger.com (JLL) — Fri, 15 Apr 2011 07:44:00 +0000

Is there evidence behind biotin and hair growth? (Photo by Martin Neuhof)

Long-time readers of the blog may remember that one of the earliest experiments I did was with biotin, also known as vitamin B7. The purpose was to see whether taking a biotin supplement would affect nail and hair strength.

I wrote back then that although a lot of people seemed to believe biotin is good for hair and nails, there were no studies showing it really did anything except in rare cases when the subject was biotin deficient. After two weeks, I posted a quick update. When I'd been taking 5 mg for a month, I concluded the experiment. As you might expect, I didn't see any results.

I've since learned that one month is way too short for any kind of results when it comes to hair growth experiments. In most cases, six months would be the minimum, otherwise you're just wasting money without really learning anything new.

A pubmed search on biotin and hair growth still doesn't come up with any interesting studies. The only thing biotin seems to be proven to do is help with uncombable hair syndrome (link):

We report a family affected to the fourth generation by uncombable hair syndrome. This syndrome is characterized by unruly, dry, blond hair with a tangled appearance. The family pedigree strongly supports the hypothesis of autosomal dominant inheritance; some members of the family had, apart from uncombable hair, minor signs of atopy and ectodermal dysplasia, such as abnormalities of the nails. The diagnosis was confirmed by means of extensive scanning electron microscopy. A trial with oral biotin 5 mg/day was started on two young patients with excellent results as regards the hair appearance, although scanning electron microscopy did not show structural changes in the hair. After a 2-year-period of follow-up, hair normality was maintained without biotin, while nail fragility still required biotin supplementation for control.

In this study, 5 mg biotin was taken daily. Even much smaller doses seem to be helpful for uncombable hair syndrome, however (link):

Three children are reported with uncombable hair syndrome, consisting of slow-growing, straw-colored scalp hair that could not be combed flat. The hairs appeared normal on light microscopy but on scanning electron microscopy were triangular in cross section, with canal-like longitudinal depressions. Oral biotin, 0.3 mg three times a day, produced significant improvement after 4 months in one patient, with increased growth rate and with strength and combability of the hair, although the triangular shape remained. The other two patients were unique in having associated ectodermal dysplasia. Their hair slowly improved in appearance and combability over 5 years without biotin therapy.

These studies confirm the fact that biotin does play a part in hair growth, and that it's possible to affect even the growth rate through biotin supplementation. Although the cause of uncombable hair syndrome is unknown, a biotin deficiency (perhaps due to genetic reasons) may play a part. On the other hand, the syndrome often improves by itself with age.

Studies like this do not really warrant supplementing with biotin if you're suffering from androgenic alopecia or just want to make your hair grow thicker and faster. And yet a lot of people seem to believe biotin will do the trick. They keep saying there's "a lot of evidence" for biotin and hair growth, but the references are missing. The actual studies are always about biotin deficiencies or like the ones I quoted above.

However, a while ago I came across one study from 1992 that actually looked at the effect of biotin supplements on hair loss. It's no wonder I didn't find it earlier, since it's not indexed in pubmed. Nor do I have access to the full paper, but here's the abstract:

An examination of the effect of biotin on alopecia and hair quality.

The effect of a daily oral dose of 2,5 mg biotin was studied in 93 patients with the symptoms hair-loss (mostly androgenetic alopecia) and reduced hair quality. The mean duration of treatment was 7,9 +/- 2,8 months. An obvious improvement of hair-loss was reported in 64%, and a slight improvement in 9%. Hair quality was clearly improved in 70% and slightly in 12%. Brittle finger nails as an additional complaint were improved in 80%. If alopecia, decreased hair quality and brittle finger nails occurred in combination, improvement was observed frequently collectively. The study allows - as already shown in a previous investigation concerning brittle finger nails - to suggest biotin as an effective and well tolerated therapy in cases of alopecia and decreased hair quality.

The majority of subjects had improvements in hair loss and hair quality from taking 2.5 mg biotin daily. Sounds good, right? Makes you wonder why nobody has attempted to repeat the experiment if the results are real. Another thing that strikes me as odd is the duration of the experiment. Why a mean duration of 7.9 months with standard deviation? Weren't all the subjects taking biotin for the same duration? Did they just quit whenever they felt like it? That just sounds like bad study design, which makes me somewhat skeptical of the results.

Still, it's intriguing enough to make me add biotin back on the supplement menu for the time being. Although a "it can't hurt and might help" mentality may be dangerous in some cases, I'm unaware of any negative side effects from taking 5 mg biotin daily. This time I'm aiming for at least six months instead of just one.

For more information on hair growth, see these posts:

Soy Isoflavones and Chili Pepper for Hair Growth – Experiment Update
Emu Oil vs. Hair Again® Topical Gel: Hair Growth Battle Conclusion
Do Flax Lignans Reduce Hair Loss from MPB?
2% Nizoral Shampoo Increases Hair Growth More than 2% Minoxidil

Soy Isoflavones and Chili Pepper for Hair Growth – Experiment Update

noreply@blogger.com (JLL) — Tue, 12 Apr 2011 09:20:00 +0000

Spicy peppers contain capsaicin, which should promote hair growth. (Photo by Jonathon W)

Several readers have been asking for an update on my hair growth experiment with soy isoflavones and capsaicin. I admit it's long overdue, so here goes!

First some background on the experiment. Why soy isoflavones? I know there are a lot of people who think soy is the ultimate poison, and while I'm not a big fan of soy as a food, the science behind isoflavones and hair growth is strong enough for me to give it a go. Soy isoflavones have been shown to increase IGF-1 in the skin, which in turn promotes hair growth. Although soy also reduces DHT in rats and in humans, the effects on IGF-1 seem to be the primary way through which isoflavones grow hair.

Capsaicin seems to have a similar effect on IGF-1, and in both mice and humans, the combination of soy isoflavones and capsaicin appears to be more effective than capsaicin alone. I have not seen a direct comparison of soy isoflavones and soy isoflavones + capsaicin, however, so it's unclear how important capsaicin really is. Nevertheless, I chose to take both for the experiment.

The participants in the study were given a capsaicin supplement, but I decided to take the natural route and just add cayenne pepper or chili powder into my food instead. It's difficult to determine just how much capsaicin I've been ingesting this way, since the capsaicin content depends on a lot of variables. As I wrote when the experiment began:

The only problem is that it's pretty difficult to estimate the amount of capsaicin; a tablespoon of ground chili will contain anywhere between 0.8 mg and 480 mg of capsaicin. In the study, 7 mg per day was consumed, so if I manage to eat a tablespoon, I should have decent odds of ingesting at least as much capsaicin.

The amount of isoflavones I've been eating, on the other hand, has been easy to measure. One capsule contains 60 mg of isoflavones, which is 15 mg less than in the study.

And what about the results? I've not taken any pictures, since unlike in the retinol experiment, there's not much visible going on. I haven't cut my hair in years, and the length of my hair is still the same as it was before (the maximum length of your hair is genetically determined), so it's safe to say that isoflavones and capsaicin haven't done anything in that department.

I also haven't seen any increase in the rate of hair growth, which is perhaps a bit surprising, since you might expect an increase in IGF-1 to increase the speed at which hairs grow. But then again, I have no reliable way of measuring my IGF-1 levels either. I've simply been looking at a few hairs and measuring how much they grow each month.

The one thing I noticed during this experiment is something of a shed in the beginning. There's no way to be sure it's the isoflavones and capsaicin working, but I haven't noticed anything similar with the other experiments. After a few months, I seemed to not only shed more hairs in general, but especially from the front of the scalp. Moreover, many of these hairs had not grown to their full length yet.

As most of you probably know, that can be a good or a bad sign. A lot hair growth drugs, including finasteride, cause an initial shed, after which the hairs grow back stronger and healthier. Then again, inflammation also causes hairs to shed earlier than they should, only they grow back weaker every time.

At this point, it's still too early to tell, since the new hairs are still growing. At least on the surface they look fine. What's funny is that there are some spots where several hairs are pretty much the exact same length. The two possible reasons is that those hairs were shed at the same time and now regrowing, or that the isoflavones and capsaicin increased the number of hair follicles. I suspect the former, but I can't be sure.

So what's the next step? I've already ordered a second bottle of isoflavone capsules, and since I like to use chili in my food anyway, I'll pretty much keep doing what I've been doing so far. If I see any dramatic changes, I will post about them, but if not, I will just consider the isoflavones and capsaicin thing a preventative measure and move on to more interesting experiments.

That's it for today. I hope you found this update useful, and if you have further questions or you've done a similar experiment of your own, please let us know in the comment section.

For more information on hair growth, see these posts:

Topical Retinoids Increase Hair Growth in Most People
BioSil, JarroSil & Beer – Silicon Experiment Conclusion
Zinc Pyrithione Reduces Shedding and Moderately Promotes Hair Growth
Eclipta Alba Extract Grows Hair Quicker than Minoxidil

Vegetable vs. Animal Sources of Vitamin A: Why Eating Carrots Isn't Enough

noreply@blogger.com (JLL) — Wed, 02 Feb 2011 11:42:00 +0000

Think you're getting enough vitamin A from carrots? Think again. (Photo by Ben Hussman)

In the comment section of my previous post on genes, diet and cavities, a couple of readers commented that vitamin A is necessary for proper dental health. I replied that I get plenty of beta-carotene (the vitamin A precursor found in vegetables and fruits) from red palm oil, which I use for most of my cooking these days.

Today, however, I came across a couple of papers looking at how well humans actually absorb beta-carotene and convert it to vitamin A (link, link). To my surprise, the conversion rate was much poorer than I'd previously thought. The first paper, which looked at beta-carotene absorption in 11 men, had this to say:

The vitamin A activity of ß-carotene is variable. The carotene in fruit, grains, and oils seems to be more effective as a source of vitamin A than that in dark-green leafy vegetables.

So, not all sources of beta-carotene are equally good in terms of absorption. The conversion rate also depends on the amount of beta-carotene (the higher the amount, the lower the rate) and whether fat is included or not.

Strikingly, only 6 of the 11 men included in the study absorbed and converted the beta-carotene they were given. The remaining 5 were classified as non-responders. The authors conclude that the vitamin A activity of beta-carotene can be "surprisingly low and variable". Even in those who did respond to supplementation, mean absorption was only ~4% and the conversion ratio was ~0.05.

In a similar study on 11 women, the same thing happened: only 6 of the women absorbed and converted beta-carotene enough to be measurable, while 5 women were non-responders. In those who did respond, mean absorption was ~6% and the conversion ratio ~0.1. This confirms earlier findings reporting that women absorb and convert beta-carotene more efficiently than men; the same also appears to be true in rats.

These figures suggest that the commonly accepted conversion rates of beta-carotene from plant sources may be too optimistic. Even red palm oil might not be up to par with animal sources. In one study, switching from green leafy vegetables to red palm oil did increase retinol levels, but only in subjects who were vitamin A deficient to begin with (link). And for many Westerners who don't eat palm oil or organ meats, the reality is even worse:

Also, it seems that the vitamin A activity of ß-carotene that is not dissolved in oil and emulsified is low and variable. Most ß-carotene in the American diet is not consumed in an emulsified form with fat. Our intent was to replicate a typical diet to develop better leads for how the body utilizes its given resources. The fat content of the meal that accompanied the doses in our study was the recommended amount, 30%. Many professionals recommend lower-fat diets.

Now there's something for the low-fat raw food vegetarians to chew on. On the other hand, the absorption of retinol, found in animal sources such as liver and eggs, appears to be much higher. Most of the estimates I've seen on various websites are between 60-90%, but even that may be too conservative, as the only actual study I could find showed that absorption was >99% (link).

Since my vitamin D levels are already good, and I take vitamin K2 supplements, the missing link in the trinity of dental health could indeed be vitamin A in my case. While I do eat eggs every now and then, their retinol content is only about 10% of that of liver. I guess it's time to put organs on the menu.

For more information dental health, see these posts:

Genes, Diet and Oral Health: Why Do Some People Get Cavities and Others Don't?
Tea, Coffee and Cocoa: All Good for Your Teeth
Dental Health Effects of Green and Black Tea
Preventing Mouth Ulcers with Tea Tree Oil Toothpaste - Results after Two Months

Genes, Diet and Oral Health: Why Do Some People Get Cavities and Others Don't?

noreply@blogger.com (JLL) — Tue, 25 Jan 2011 10:57:00 +0000

Getting rid of candies didn't prevent me from getting caries. (Photo by exper)

As you may know, I have something of an ongoing experiment with dental health. This includes reducing cavities, preventing gingivitis and the receding of gums, and also finding safe ways of whitening teeth.

In previous updates, the main focus has been on the teeth whitening aspect. The last product I purchased was called "Plus White 5 Minute Bleach Whitening Gel". Compared to the supposedly teeth whitening toothpastes out there, this product does seem more effective.

However, in recent months, I've noticed increased sensitivity along the gumline. Specifically, the gums next to two of my upper teeth seem to be the problem. The whitening gel probably has very little to do with it, but it doesn't solve the problem either. In the short term, whitening gels can increase sensitivity, so for the time being, I've turned my focus elsewhere – to preventing caries and improving gum health.

The motivation for this post is that I've struggled with these things my whole life, and despite my various experiments with diet, I've yet to find a proper solution to the problem. When I was a kid, the common explanation was that too much candy and soda was the reason for dental cavities – despite the fact that scientists had already shown that carbohydrates in general give rise to the bacteria that cause caries. So when I got a bit older, I cut back on candy and soda, hoping it would be enough.

Unfortunately, it wasn't. Apart from the Snickers Bars and Coca-Cola I'd occasionally enjoyed that were now gone, my diet remained the same. It took me a long time to discover that all carbs are essentially sugars, that all acidic drinks make the issue worse, and that it's not just Coke and candy that are the problem. You can get cavities just as easily by eating bread and drinking apple juice. Then it was time to get rid of those too.

When I reduced my carb consumption and switched to a more paleo-like diet, my dental health improved, but it still didn't stop me from getting a new cavity every now and then. Furthermore, I knew several people who ate junk food and drank acidic sodas all the time, and yet had never had cavities. Some didn't even brush their teeth every day, let alone floss. When we were kids, my brother and I had very similar diets, and yet I was the only one to get cavities.

These things have led me to believe that genes play a more important part than most dentists would have you believe. Kind of like some people stay thin no matter how much they eat. But, just like in the case of weight loss, your genes do not necessarily determine your fate – it just means you have to know what you're doing. People who don't have the genes for staying naturally thin have to be more careful with what they eat if they want to avoid weight gain. Similarly, people who get cavities easily have to be more careful with dental health.

While keeping your teeth clean by brushing, flossing and chewing gum prevents cavities, I'm wondering whether all the cleaning really strikes the problem at the root (no pun intended). If genetics do play a role, what is it specifically about some people's genes that keeps them from getting cavities, despite their poor dental health habits?

One important factor in cavity formation is saliva. The surfaces of teeth are constantly going through a process of demineralization and remineralization. The balance depends, in part, on salivary flow and the pH of saliva, with the mineral content probably playing a role as well. I know my mouth often feels kind of dry and acidic, which can't be a good thing for remineralization. What is unclear to me is how to affect these things.

There are a million websites out there listing foods that are "acid-forming" or "alkaline-forming", but the classification seems very unscientific. Some list apples as acid-forming because apples themselves are acidic, some list them as alkaline-forming because they claim we should look at what happens after digestion. Here's a quote from one such website:

All foods are "burned" in the body -- more commonly called "digested" -- leaving an ash as the result of the "burning", or the digestion. This food ash can be neutral, acid or alkaline, depending largely on the mineral composition of the foods.

I'm not sure how scientifically valid this theory is in the first place, but I do know that even those who promote the "food ash" theory disagree on which foods leave acid or alkaline ash. One person will tell you plums are acid-forming, while others will tell you they're alkaline-forming. I doubt any of them have actually burned plums and studied the ashes.

So, expect some dental health related posts in the upcoming weeks and months, as I go through some of the papers on the subject. I'm also interested in hearing your comments, especially if you've previously suffered from cavities but managed to find a solution.

Meanwhile, for more information on dental health, see these posts:

Tea, Coffee and Cocoa: All Good for Your Teeth
Dental Health Effects of Green and Black Tea
The Role of Coenzyme Q10 in Oral Health
Whitening Teeth & Healing Gums: In Search of the Perfect Toothpaste

Green Tea as a Pro-oxidant: Too Much of a Good Thing?

noreply@blogger.com (JLL) — Mon, 10 Jan 2011 11:13:00 +0000

Is too much green tea harmful for you? (Photo by tornado_twister)

I was browsing through the latest studies on green tea and came across a paper saying EGCG, one of the green tea polyphenols, increases protein cross-linking (link). I was intrigued, because this was the first time I'd heard of such an effect. The abstract also mentions that there's increasing evidence EGCG can generate reactive oxygen species and break DNA strands in biological systems. In effect, it says that the antioxidant is actually a pro-oxidant.

I looked up some of the references and indeed, even green tea's polyphenols (at least EGCG, possibly some others) have oxidative effects under certain in vitro conditions. For example, in human whole blood lymphocytes, EGCG either suppresses or induces DNA strand breakage, depending on the concentration.

In concentrations between 0.01-10 μM (micromoles/L), strand breakage decreases, but once the concetration gets higher than 1000 μM, it increases instead. In purified blood lymphocytes, concentrations of 1-100 μM induce and concentrations of 0.01-0.1 μM suppress DNA strand breakage.

Sounds an awfully lot like hormesis, doesn't it? As with everything, the dose makes the poison. The interesting part, of course, is whether drinking green tea can cause similar harmful effects in real life.

Luckily, one study looked at the effect of green tea on DNA strand breaks in rats (link). The smaller dose (which according to the authors is equivalent to one desiliter of green tea in humans) had no effect, but the larger dose (equivalent to half a liter) significantly reduced strand breaks.

Half a liter of green tea, equal to about three cups, increase total plasma antioxidant capacity only moderately. When only EGCG is taken into account, the results vary somewhat from study to study, but concentrations rarely exceed 1 μM (link). Also, plasma antioxidant activity has a plateau, which suggests that the absorption mechanism of green tea polyphenols becomes saturated after a certain point:

To make the tea used in the study, 500 ml of boiling water was poured on 20 grams of green tea leaves (8-10 tea bags), and the tea was then allowed to infuse for 10 minutes. That makes for a very strong tea, much stronger than the ones used in the other studies. The volunteers drank 300-400 ml of the tea, after which blood samples were collected at different time intervals

In this study, there was no difference between those who drank 300 and 400 ml of the tea. Even then, the increase in antioxidant activity was only 4% at the peak. Thus, it seems unlikely that harmful levels could be reached by simply drinking plenty of green tea. In one Asian population, 10 cups of green tea daily reduced total mortality compared to those who drank less green tea and/or smoked.

Theoretically at least, extracts and supplements could be a different matter, because they often contain a higher percentage of EGCG than green tea and come with things that increase absorption. For example, piperine increases plasma levels of EGCG.

One green tea extract containing 40% EGCG resulted in a peak of 0.8 μg/mL in human subjects; when the same extract was complexed with phospholipids, the peak was 1.9 μg/mL. If my calculations are correct (which they often aren't; please correct me if I'm wrong), then these would be ~1.75 μM and ~4.14 μM, respectively. Again, in whole blood lymphocytes concentrations between 0.01-10 μM, strand breakage was decreased, and it took concentrations higher than 1000 μM to increase strand breakage.

All in all, it appears that green tea in reasonable quantities (at least up to 10 cups) does not cause it to act as an oxidant in vivo. It's unknown what a much higher amount would do, assuming you could somehow bring yourself to drink 50 cups. I haven't seen any human studies on such amounts. But if the plateau effect is indeed true, then you might not be able to reach high plasma levels of EGCG no matter how much you drink.

With supplements, the situation is different. Piperine and phospholipids make reaching higher plasma values possible, which can be a good thing or a bad thing, depending on what you're using the supplements for. Some conditions require higher doses than others, so you'll have to judge the proper approach on a case by case basis. However, since EGCG does have the potential of being a pro-oxidant in vitro and is toxic to the liver in very high amounts, be careful not to overdo it with green tea supplements.

For more information on green tea and health, see these posts:

Green Tea Protects from the Psychological Effects of Stress in Rats
Tea, Coffee and Cocoa: All Good for Your Teeth
Green Tea and Capsaicin Reduce Hunger and Calorie Intake
Green Tea Catechin Reverses the Effect of DHT in Prostate Cancer Cells

Dark Chocolate Reduces Blood Pressure and Improves Insulin Sensitivity in Just Two Weeks

noreply@blogger.com (JLL) — Wed, 05 Jan 2011 11:48:00 +0000

Not all things that are good for you taste bad. (Photo by CC Chapman)

Everyone knows that dark chocolate is healthy, but how many of us really know why exactly it's healthy? It's the same as with red wine: it's common knowledge that it's healthy – it contains those magical polyphenols, after all – but the actual effects are mentioned less frequently.

Most things that are labeled healthy by mainstream media are things that reduce the risk of cardiovascular disease. The same is true of red wine and dark chocolate, although I'm sure there's more to them than just heart health. Resveratrol, found in red wine, for example has a multitude of effects. What I found interesting, however, is how quickly dark chocolate can have a beneficial effect on two common health problems: blood pressure and glucose intolerance (link).

Study design

To study how dark chocolate affects glucose tolerance, insulin sensitivity and blood pressure, 19 subjects with hypertension and impaired glucose tolerance were chosen for the experiment. Smokers and those with significant overweight (BMI > 30) or diabetes were excluded.

The subjects were then randomized and given either 100 grams of flavonol-rich dark chocolate or flavonol-free white chocolate for 15 days. They were told to eat the chocolate in two 50 gram doses, one for breakfast and one for lunch. After a washout period of one week the two treatments were switched, so that those who had been eating dark chocolate got white chocolate instead and vice versa.

Results

Two weeks of dark chocolate consumption decreased insulin resistance significantly compared to baseline and white chocolate. The graphs below show the results from various measurements.

The graph on the left show the results from the homeostasis model asssessment of insulin resistance (HOMA-IR) for baseline, flavonoid-rich dark chocolate (FRDC) and flavonoid-free white chocolate (FFWC). The three other graphs show the differences in insulin sensitivity. White chocolate had no effect on any of the tests, while dark chocolate improved glucose and insulin responses to the oral glucose tolerance test.

Compared to baseline, blood pressure decreased after dark chocolate consumption. White chocolate had no effect on 24-h, daytime or nighttime blood pressure. The graphs below show the changes in systolic and diastolic blood pressure.

Dark chocolate also increased flow-mediated dilation, which measures endothelial function. Again, white chocolate had no effect compared to baseline. Interestingly, dark chocolate also reduced LDL cholesterol compared to baseline and white chocolate but had no effect on triglycerides and HDL.

Conclusion

In people with hypertension and impaired insulin sensitivity, dark chocolate (but not white chocolate) reduced blood pressure and improved glucose tolerance and insulin sensitivity. Endothelial function was also improved.

What's interesting about this study is that the duration was so short: the participants saw improvements in just two weeks. And, unlike in many studies, they weren't given cocoa powder or a small dose of dark chocolate, but an entire 100 gram chocolate bar for each day. Also, the subjects were not diabetic, and they only had stage 1 hypertension (systolic 140-159 mmHg, diastolic 90-99 mmHg), which suggests that dark chocolate is helpful even before things get really bad.

I try to keep my intake at around 50 grams per day on average, but at least this study shows that higher amounts are not bad for cholesterol, blood pressure or insulin sensitivity. The reasons I try to stay below 100 grams are the high iron and copper contents and possible lead contamination in cocoa powder.

Still, if you're eating milk chocolate with a low cocoa content (typically around 30%), consider upping the ante and slowly progressing towards darker chocolates. It's the better choice in at least five different ways.

For more information on blood pressure, insulin and cholesterol, see these posts:

Hibiscus Tea Increases HDL, Lowers LDL and Triglycerides
The Many Health Benefits of Rooibos Tea
Intermittent Fasting Improves Insulin Sensitivity Even without Weight Loss
Intermittent Fasting with a Condensed Eating Window – Part III: Fasting Blood Glucose, Cortisol & Conclusion

Nootropics, Longevity and More: The Year 2010 in Review

noreply@blogger.com (JLL) — Mon, 03 Jan 2011 12:25:00 +0000

Comments or suggestions for the year 2011? Drop a comment! (Photo by Altus)

Happy New Year everyone! I hope your holidays went well and you're ready to make 2011 even better than last year. But before we do that, let's take a look at some of the best bits and pieces from 2010.

In January, I finally got a chance to see Aubrey de Grey for the first time. His presentation in Helsinki, Finland was mostly familiar to me already, but I enjoyed it nonetheless. Perhaps the most interesting part was when the audience got to ask questions; I thought Aubrey's answers were good, especially given that some of the comments were pretty frustrating (apparently some people think going through their entire family history somehow qualifies as a question). If you want to check out the presentation, the video is still available online through the link above. And in case you want to know more about Aubrey himself, he was also interviewed in Wired.com a while ago.

Nootropics are gaining more and more attention these days. Even 60 minutes ran a segment on students boosting brain power to do better in their studies. Amphetamine derivatives are still the most popular choice – but whoever comes up with an "organic herbal formula" that actually works as well as Adderrall is going to be rich. I also did an experiment with Ashwagandha to see whether it had a nootropic effect. It didn't, at least not the brand I was using.

And then there was the experiment with BioSil, the stuff that is supposed to make your hair and nails stronger. The science seems solid, but as I wrote in my conclusion, the price of the liquid supplement doesn't seem worth it, since orthosilicic acid, the active ingredient, is also present in my favourite beverage.

Speaking of hair, a lot of people have asked for an update on the soy isoflavones + capsaicin experiment, another one of my attempts at finding a magical hair growth formula that will make me filthy rich. The experiment has been going on for six months now, which is longer than the five months that the original study lasted, so perhaps a proper update is indeed due. So far I haven't seen much visible changes, however. I'm now adding various kinds of chili powders and pastes to almost all my foods, but I'm thinking of ordering capsaicin supplements to be sure I'm getting enough to match the study. And I also need another bottle of soy isoflavones.

I've tried a lot of useless supplements and topicals, but last year I came across something that really, actually works: retinoids. I've now been using them for over a year and I can really see the difference. My advice to anyone looking for real results is to forget about all the overpriced skin creams that are really nothing but moisturizers and go for tretinoin instead. Of course, since it actually works it's prescription stuff, so you can't just buy it from the store, you'll have to order it online and hope your package doesn't get confiscated by the customs officers who surely know better what you need than you do. Thank god for regulations!

Probably the longest and most throrough post of last year was about human hibernation and how it might relate to longevity. In addition to a look at the current state of hibernation science, there's also the odd legend of lotska, the art of hibernation allegedly practiced by poor Russian peasants:

At the first fall of snow the whole family gathers round the stove, lies down, ceases to wrestle with the problems of human existence, and quietly goes to sleep. Once a day every one wakes up to eat a piece of hard bread, of which an amount sufficient to last six months has providently been baked in the previous autumn. When the bread has been washed down with a draught of water, everyone goes to sleep again. The members of the family take it in turn to watch and keep the fire alight.

And of course, no post on slowing down metabolism would be complete without Indian fakirs and frozen mountain climbers. Check it out if you have the time, it's fascinating stuff.

While the Russian peasants may have spent most of their winter sleeping to avoid starving, there are also those who can eat as much as they like and still avoid getting fat. Even without any exercise. I'll let other bloggers fight it out over the details of the energy equation and whether a calorie truly is a calorie, but take a look at the BBC documentary in the link to see what I mean. Also check out the comment section, some interesting anecdotes in there.

How is the life extension movement doing these days? Well, the same old (and false) arguments against longer lifespans are still there, but the overall mood is pretty optimistic. Personally, I've noticed that younger people tend to be more open to the possibility of life extension than middle-aged people. Go figure. Meanwhile, the Russians have apparently found the cure for aging, although I haven't heard anything new on SkQ1 since September. But that's okay, because the next fountain of youth is already here.

Long-time readers of this blog probably remember that I did intermittent fasting for over a year. Part of the reason was that I wanted to see if 24-hour fasts could be done – I wanted to be the master of my hunger, so to speak. However, the most important reason were the studies showing positive effects from intermittent fasting without restricting total calories. You know, the whole "cleaning cells from junk through autophagy" thing.

But alas, after going through the studies more carefully, I was disappointed to find out that whenever intermittent fasting increased lifespan in mice, total calories had also been restricted. In effect, intermittent fasting extends lifespan only in conjuction with caloric restriction. Some of the other benefits of fasting may still be valid, to a degree at least, but without potential gains in lifespan, I don't see the point in doing a strict 24/24-hour cycle of fasting and feasting anymore. Besides, I now think that even full-blown calorie restriction would only give me a few extra years. Why? Because humans just can't do CR the same way rodents can. More on this later. Meanwhile, see my updated health regimen.

Of course, there were also several other posts which I didn't mention here; see the archives section in case you missed them. And just so you don't miss anything interesting in the future, remember to subscribe to my feed and to follow me on Twitter, which I use to post stuff (life extension, health, science) I don't have time to blog about in depth. Oh yeah, and tell your friends to do so too!

For summaries of previous years, see these posts:

10 Human Experiments of 2009 – Year in Review
7 Human Experiments of 2008 – Year in Review